Cardiovascular Notes

Ftplectures Cardiovascular system Lecture Notes
CARDIOLOGY
Medicine made simple
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Ftplectures Cardiovascular system
Copyright 2014

Adeleke Adesina, DO
Cardiovascular system

2012 ftplectures LLC
1133 Broadway Suite 706,
New York, NY, 10010

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678&)$#9&: 3-/ %&./2#2;' Leaining the pathophysiological anu clinical featuies of
acute myocaiuial infaiction, as well as tieatment options.

<&3#2#$#-2:' Acute myocaiuial infaiction is neciosis of myocaiuium uue to massive
ischemia causeu by coionaiy aiteiy occlusion. It is the most common cause of the
ueath in the 0niteu States (Su% moitality).

=.*:&:> ?#:@ 3.)$-/:'
Acionym: FLASB - NB
Family histoiy
Low BBL
Age (men>4S, women>SS)
Smoking
Bypeitension
Nale genuei
Biabetes

A.$B-CB,:#-%-;,' Acute myocaiuial infaiction iepiesents the neciosis of some
paits of heait muscle which happens uue to the massive ischemia causeu by
complete occlusion of the coionaiy aiteiy iesponsible foi supplying that iegion.

=%#2#).% :,DC$-D: .20 :#;2:
Chest pain (ciushing; iauiation to the neck, jaw, anu left aim)
Nausea
vomiting
Biaphoiesis
Shoitness of bieath
Weakness, fatigue
Symptoms last moie than Su minutes.
Atypical clinical pictuie in:
Biabetics
Elueily
Women
St. post suigeiy

<#.;2-:#:
EKu changes (ST-elevation, Q-waves (at least u.u4s anu 2S% of R wave), T-
waves inveision
o I, avL, vS, v6 - lateial wall
o v1, v2, vS - anteiioi wall
o II, III, avF - infeiioi wall
o v1, v2 - Septal wall
Caiuiac enzyme
o CK-NB (incieases uuiing the fiist 4-8 houis; ietuins to noimal values
aftei 48-72 houis)
o Tioponin IT (incieases in the fiist S-S houis; ietuins to noimal
values aftei S-14 uays)
* CK-NB is an impoitant maikei foi ieinfaiction

=-DC%#).$#-2:
ventiiculai fibiillation
Reinfaiction

"/&.$D&2$
Noiphine
0xygen
Nitiates
Aspiiin - antiplatelet (aspiiin uecieases moitality)
Beta-blockeis (ieuuce moitality)
ACE inhibitois
Statins
Anticoagulant - Low moleculai weight hepaiine
Revasculaiization
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012&)$#3&/ 45, %&-,6#67' Leaining clinical signs, uiagnostic techniques, anu
tieatment options foi acute peiicaiuitis.

8&4#6#$#56/' Peiicaiuitis is an inflammation of peiicaiuium.

9-*/&/: ;#/< 4-)$5,/'
Iuiopathic
viiuses (Coxsackie B, BIv, Echoviiuses)
Rauiation
0iemia
Acute myocaiuial infaiction (Biesslei's synuiome)
Lupus
Amyloiuosis
Rheumatoiu aithiitis
Saicoiuosis
Piocainamiue, hyuialazine, izoniaziue (uiug inuuceu peiicaiuitis)

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Retiosteinal chest pain (pleuiitic pain which iauiates to tiapezius oi
scapula)
o Leaning foiwaiu loweis the pain.
o Swallowing, cough, anu lying uown inciease the pain.
Fevei
Peiicaiuial iub

8#-765/#/
EKu
o Biffuse S-T elevation
o P-R uepiession (the most specific foi peiicaiuitis)
o T wave inveision
Echocaiuiogiam

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Peiicaiuial effusion
Peiicaiuial tamponaue

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Aspiiin
Steioius aie given if the patient uoes not iesponu well to aspiiin
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!"#$%&'($) +,- .$/-0'012 ueflnlLlon, aLhophyslology, Causes/ 8lsk facLors, Cllnlcal sympLoms
and slgns, ulagnosls and 1reaLmenL.
3$+'0'&',02
4/&5,657)',.,17
SLenoLlc aorLlc wall causes lefL venLrlcular ouLflow obsLrucLlon. valve belng sLenoLlc becomes
unable Lo push blood Lo lefL venLrlcle. uecrease Lv ouLflow leads Lo lefL venLrlcular hyperLrophy
due Lo excesslve amounL of force hearL has Lo puL Lo pump Lhe blood. Cver a passage of Llme
Lv dllaLaLlon and Lhen mlLral regurglLaLlon develops. Cardlac ouLpuL becomes decrease.
8/9)$): ;')< +/%&,-)2
CalclflcaLlon of Lhe blcuspld valve (olderly paLlenLs mosL develop calclflcaLlon of Lhe valve due
Lo deposlLlon of calclum)
PlsLory of rheumaLlc fever
8.'0'%/. )7=6&,=) /0> )'10)2
?7=6&,=)2
AsympLomaLlc for years
WlLh Lhe worsenlng of obsLrucLlon
Syncope
Anglna
uyspnea due Lo CPl
?'10)2
Murmur
Crescendo-decrescendo murmur. Can be heard aL second lnLercosLal space and caroLld
arLery
S4 sound
arvus eL Lardus a decreased or delayed caroLld sLroke
3'/10,)')
ChesL-x-ray
Lchocardlogram (Lv and LA enlargemenL)
Cardlac caLherlzaLlon: lL ls a deflnlLe dlagnosLlc LesL and gradlenL and valve area less
Lhan 0.8 ls consldered normal.

@9'A

1. A 37 year old paLlenL presenLs wlLh complalnLs of Syncope, chesL paln on physlcal exerLlon
and malalse. Cn examlnaLlon a murmur ls presenL over second lnLercosLal space. S4 sound
ls also heard. Pe has a prevlous hlsLory of rheumaLlc fever. WhaL ls Lhe llkely dlagnosls?
A. AorLlc sLenosls
8. AorLlc regurglLaLlon
C. MlLral sLenosls
u. MlLral regurglLaLlon
1he correcL answer ls: A
1he hlsLory, cllnlcal plcLure and physlcal examlnaLlon all polnL Lowards Lhe developmenL of
aorLlc sLenosls ln Lhls paLlenL. 1he murmur of aorLlc sLenosls ls usually heard aL second
lnLercosLal space. S4 sound ls promlnenL here. 8heumaLlc fever ls Lhe mosL common cause of
aorLlc sLenosls ln Lhe adulL paLlenL.
ln case of aorLlc regurglLaLlon S3 sound ls heard whereas Lhe murmur of aorLlc regurglLaLlon ls
heard aL Lhlrd lefL lnLercosLal space.
MlLral sLenosls ls characLerlzed by Lhe loud flrsL hearL sound and Lapplng apex beaL. 1he
murmur of mlLral sLenosls ls heard aL Lhe aplcal reglon and ls low-plLched.
1he murmur of mlLral regurglLaLlon ls besL heard aL Lhe apex of Lhe hearL. Pere flrsL hearL
sound ls sofL. 1he mosL common cause of mlLral regurglLaLlon ls mlLral valve prolapsed.

2. Whlch of Lhe glven opLlon ls relaLed Lo Lhe aorLlc sLenosls?
A. ulasLollc murmur
8. ALrlal flbrlllaLlon
C. 8lghL hearL fallure
u. SysLollc e[ecLlon murmur
1he correcL answer ls: u
SysLollc e[ecLlon murmur ls relaLed Lo Lhe aorLlc sLenosls. 1hls murmur ls Lhe due Lo LurbulenL
flow of blood forward across Lhe rlghL venLrlcular ouLflow LracL, aorLlc valve, or vla Lhe aorLa. lL
ls also relaLed Lo pulmonary sLenosls.
ulasLollc murmur has no relaLlon Lo Lhe aorLlc sLenosls. ulasLollc murmurs begln aL or afLer S2
hearL sound and remalns Llll aL or before S1.
AorLlc sLenosls does noL lead Lo aLrlal flbrlllaLlon buL mlLral sLenosls can cause Lhe developmenL
of aLrlal flbrlllaLlon.
8lghL hearL fallure may resulL wlLh aorLlc sLenosls buL when dlsease ls qulLe old so besL opLlon ls
u.

3. A 43-year-old paLlenL presenLs wlLh conflrm dlagnosls of aorLlc sLenosls. Pe has a hlsLory of
fever and [olnL palns. WhaL would be Lhe mosL llkely cause here?
A. 8acLerlal endocardlLls
8. CongenlLal blcuspld valve
C. 8heumaLlc fever
u. Marfan's syndrome
1he correcL answer ls: C
AorLlc sLenosls ln an adulL ls usually Lhe resulL of rheumaLlc fever. 8heumaLlc fever ls
an lnflammaLory condlLlon LhaL precedes an lnfecLlon by Lhe "#$%&#'('(()* &+',%-%*. lL can
lnvolve Lhe skln, hearL, braln and [olnLs.
A congenlLal blcuspld valve ls baslcally a congenlLal dlsease vulnerable Lo endocardlLls and
ulLlmaLely develops calclflcaLlon as well as sympLomaLlc sLenosls.
AorLlc sLenosls ls usually seen afLer Lhe bacLerlal endocardlLls. 1here musL be a hlsLory of
developmenL of bacLerlal endocardlLls.
Marfan's syndrome can cause aorLlc sLenosls buL LhaL adulL musL have Lhe feaLures of Marfan's
syndrome.

4. Crescendo-decrescendo ls Lhe murmur found ln aorLlc sLenosls. WhaL ls lLs exacL locaLlon?
A. llfLh lnLercosLal space
8. Second lnLercosLal space and caroLld arLery
C. ln Lhe fourLh lnLercosLal space medlal Lo mld-clavlcular llne.
u. AL Lhe apex of Lhe hearL
1he correcL answer ls: 8
Slnce Crescendo-decrescendo murmur occurs due Lo sLenosls of aorLa, so lLs locaLlon would be
where aorLa ls presenL. 1he correcL answer Lherefore ls second lnLercosLal space and caroLld
arLery. All oLher opLlons are noL correcL.
3. Syphllls ls Lhe lnfecLlon whlch can cause hearL dlsease. WhaL ls Lhe mosL common valve of
Lhe hearL lnvolved by lL?
A. MlLral valve
8. ulmonary valve
C. AorLlc valve
u. 1rlcuspld valve
ln Lhe laLer sLages of dlsease, syphllls lnvolves Lhe hearL and remalns conflned Lo Lhe base of
Lhe aorLa. When lL lnvolves Lhe wall of Lhe aorLa, syphllls leads Lo loss of Lhe elasLlc properLles
of Lhe aorLa and even Lhe formaLlon of aorLlc aneurysms.
MlLral valve, pulmonary valve and Lrlcuspld valve are noL affecLed by Lhe syphllls.

!"#$%& '#(")$ +%,#)$ -%.%/# 0'+-1

"#$%&'()%* +,- .%/-0(012 ueflnlLlon, aLhophyslology, Cllnlcal sympLoms and slgns, hyslcal
Lxam, ulagnosls, CompllcaLlons, and 1reaLmenL.

3%+(0('(,02
1he defecL beLween Lhe Lwo aLrla ls called aLrlal sepLal defecL. 1here are Lwo Lypes:
"*'(45 6-(5452 1he llLLle hole aL Lhe Lop beLween Lhe rlghL and Lhe lefL aLrlum ls called osLlum
prlmum. 80 sepLal defecLs are osLlum prlmum.
7%6'45 6-(5452 lL ls Lhe defecL aL Lhe lower slde beLween Lhe rlghL and Lhe lefL aLrlum.

8/4*%*9 :(*; +/&',-*2

</'=,6=>*(,.,1>
ueoxygenaLed blood normally comes from Lhe head and Lhe lower slde of Lhe body lnLo Lhe
superlor vena cava (SvC) and lnferlor vena cava (lvC) respecLlvely. lrom here lL enLers lnLo Lhe
rlghL aLrlum. 8lghL aLrlum now has deoxygenaLed blood whlch enLers lnLo Lhe rlghL venLrlcle.
8lghL venLrlcle conLracLs durlng sysLole and pumps blood lnLo Lhe pulmonary arLerles whlch
now enLers lnLo Lhe lung. 1he pulmonary arLerles become smaller pulmonary caplllarles whlch
Lake oxygen, exchange wlLh carbon dloxlde. now oxygenaLed blood ls Laken up by Lhe
pulmonary velns lnLo Lhe lefL aLrlum. 1he lefL aLrlum always has oxygenaLed blood.
ln case of aLrlal sepLal defecL Lhe lefL aLrlum cannoL pump blood lnLo Lhe lefL venLrlcle. 1he
oxygenaLed blood ls noL Lransferred Lo Lhe whole of Lhe body Lhrough aorLa. 1hus, oxygen ls
noL LransmlLLed Lo Lhe body.
1he pressure from Lhe lvC and SvC comlng lnLo Lhe rlghL aLrlum ls always aL low slde. 1he
pressure ln Lhe 8v ls 23/10 mmPg, ln Lhe lefL aLrlum ls 12 mmPg and ln Lhe lefL venLrlcle ls
130/80 mmPg.

8.(0(&/. *>56',5* /0? *(10*
1he paLlenLs are normally asympLomaLlc. 8uL as Lhe paLlenLs reach Lo 40 years of age, Lhey
develop:
uyspnea aL exerLlon
Lxerclse lnLolerance
Anemla
laLlgue

<=>*(&/. @A/5
Mld-sysLollc e[ecLlon murmur ls heard aL pulmonary area.
Wlde flxed spllL S2 sound
ulasLollc rumble ln Lhe Lrlcuspld reglon
lrregularly lrregular hearL raLe
no p waves on LkC
ALrlal flbrlllaLlon

3(/10,*(*
1ransesophageal Lchocardlogram (1LL)
ChesL x-ray
LlecLrocardlography (LkC)

8,56.(&/'(,0*
ulmonary hyperLenslon
8lghL venLrlcular fallure
Llsenmenger's dlsease
aradoxlcal emboll
SLroke

B-%/'5%0'
Surglcal repalr - close up Lhe valve
!"#$%& ($))* +,%--.,% /%0.$1#")2 3& (1,),%4%5#), +1#6718

9:;%4#"<%- =), >%1,2"20& Mean arLerlal blood pressure, normal blood pressure, aLhways
and neural aLhways.
?%12 @,#%,"1$ ($))* +,%--.,%
Mean arLerlal blood pressure: 2 (dlasLollc blood pressure) + sysLollc blood pressure / 3.
normal blood pressure ls less Lhan 120/80 mmPg l.e. sysLollc blood pressure over dlasLollc
blood pressure.
+1#6718-
1here are Lwo paLhways
neural paLhways ! fasL ! sympaLheLlc
Pormonal paLhways ! slow ! 8enln-angloLensln, aldosLerone paLhway
A%.,1$ +1#6718-
When someone ls bleedlng, lL causes decrease ln lnLravascular volume. 1he blood pressure also
decreases. normally, Lhe aorLlc arch and barorecepLors feel Lhe sLreLch ln Lhe walls of Lhe
caroLld slnus. 1hey also sense Lhe decrease ln blood pressure. Clossopharyngeal nerve of Lhe
herlng's nerve ln Lhe caroLld slnus afLer senslng Lhls sends slgnals Lo Lhe bralnsLem.
AuLomaLlcally, Lhe decrease ln parasympaLheLlc Lone ls achleved whlle lncrease of sympaLheLlc
Lone occurs Lo compensaLe Lhe decrease ln blood pressure. SympaLheLlc nervous sysLem acLs
on Lhe SA nodes and causes:
lncrease ln Lhe hearL raLe
lncrease ln Lhe conLracLlllLy of cardlac muscles
lncrease ln sLroke volume
All Lhls evenLually lncreases Lhe cardlac ouLpuL and flnally Lhe 8. 1he sympaLheLlc sysLem also
acLlvaLes Lhe alpha and beLa recepLors ln Lhe vasculaLure leadlng Lo vasoconsLrlcLlon and
lncrease ln LoLal perlpheral reslsLance (18). lncrease ln 18 leads Lo lncrease ln 8.

!"#$%$&" ()#" *$(+,"

"#$%&' ()*+#), ")-./0)+&

123&,$#4&5 6/* %&)*0#07' 0nueistanuing the basics of caiuiac tamponaue
pathophysiology, clinical featuies, uiagnosis, anu tieatment.

8&6#0#$#/0' Caiuiac tamponaue is impaiieu ventiiculai filling uue to excessive
peiicaiuial effusion.

()95&5: ;#5< 6),$/*5'
Penetiation of the chest
Iatiogenic uamage to the atiial oi ventiiculai wall uuiing cential venous
cathetei placement oi peiicaiuiocentesis
Peiicaiuitis
Nyocaiuial infaiction

=)$>/.>?5#/%/7?'
The iate of effusion is impoitant foi the uevelopment of caiuiac tamponaue.
If moie than Suu mL of fluiu aie iapiuly going into the peiicaiuial space, it
will cause tamponaue. 0n the othei hanu, in cases of slow filling, the
peiicaiuium has time to stietch so theie can be 1.S L of fluiu in peiicaiuial
space befoie ueveloping a tamponaue.
Impaiieu ventiiculai function leaus to uecieaseu pieloau, which then leaus
to low caiuiac output. Consequently, the bloou piessuie is going to be low.
The piessuies in all foui caiuiac cavities is going to be equal.

(%#0#,)% 5?-.$/-5 )0+ 5#705
Beck's tiiau:
o }vB
o Bypotension
o Nuffleu heait sounus
Naiioweu pulse piessuie (uue to low stioke volume)
Pulsus paiauoxus (bloou piessuie ueciease foi >1ummBg uuiing
inspiiation)
Tachycaiuia
8#)70/5#5
Echo
Chest X-iay
o Incieaseu caiuiac silhouette
o Cleai lung fielus
EKu
o Electiical alteinans
Caiuiac catheteiization
o Incieaseu intiathoiacic piessuie
o RA piessuie is uecieaseu with the loss of Y uescent

"*&)$-&0$
o If the patient is stable anu theie is no bloou - just watch
o If the patient is unstable - peiicaiuiocentesis
o Suigeiy if the vasculatuie walls aie uamageu
!"#$%& ()*+"), !-./*0& 123/.)0
456%,#"7%0 8/* $%)*9"9:& "#$%& '( )*+,-*. "/01+2 31&4 )10015 6+-0*+# 7-8%+ )*5.%+2 31&4
)10015 7-8%+ )*5.%+2 31&4 )10015 9+*-5 )*5.%+

!2;%0 /8 ()*+"), !-./*
:; 3#<10*&
=; >?*@,10#10*&

"?% 01&4 .10015 $+-0*+# .*+,-*. 4/01+ 1( *,/A4& -& *4+-*A 0#<10*&; 6*4-%54& $+%&%54 B-4?
&#5.1$% @%.*/&% 4?-& *4+-*A 0#<10* .*/&%& @*AA 8*A8% %((%.4 -5 4?% A%(4 *4+-/0; C/% 41 4?% 4/01+
@A11, .*5514 D%4 -541 4?% A%(4 8%54+-.A% @%.*/&% 4?-& 4/01+ &%*A& /$ 4?% 0-4+*A 8*A8%2 .*/&-5D *
,%.+%*&% -5 4?% A%(4 8%54+-./A*+ *5, ,-*&41A-. 81A/0%; "?% .*+,-*. 1/4$/4 *A&1 ,%.+%*&%&2
$%+(/&-15 *A&1 ,%.+%*&%& *5, 4?% @+*-5 D%4& *((%.4%,2 4?%+%(1+% A%*,& 41 &#5.1$%;

! E5 .?-A,+%5 4?% 01&4 .10015 $+-0*+# 4/01+ 1( ?%*+4 -& >?*@,10#10*&; "/@%+1/& &.A%+1&-&
-& 4?% 01&4 .10015 ,-&%*&% *&&1.-*4%, B-4? 4?-& 4/01+;
! "?% 01&4 .10015 $+-0*+# A-8%+ .*5.%+ -& 4?% ?%$*41.%AA/A*+ .*+.-510* (+10 A-8%+ .-++?1&-&;
! "?% 01&4 .10015 A-8%+ .*5.%+ -& 4?% 0%4*&4*&-& /&/*AA# (+10 0%A*510* 1+ A#0$?10*;
! "?% 01&4 .10015 @+*-5 .*5.%+ -& 4?% 0%4*&4*&-& /&/*AA# (+10 0%A*510* 1+ A#0$?10*;

!"#$%& ()*+",-%."/ 01,/2

345%/#"6%7 8,* $%)*.".-& ueflnlLlon, Causes, Cllnlcal sympLoms and slgns, ulagnosls,
1reaLmenL, lnLra aorLlc balloon pump (lA8).
9%8"."#",.&
Cardlogenlc shock ls Lhe decrease ln cardlac ouLpuL LhaL leads Lo decrease ln Llssue perfuslon.
1hls ls due Lo lnsufflclenL clrculaLlon of blood owlng Lo fallure of Lhe venLrlcles of Lhe hearL Lo
work effecLlvely.
We know LhaL
Mean arLerlal pressure = CC x 18
CC= cardlac ouLpuL
18= 1oLal perlpheral reslsLance
WlLh decrease ln cardlac ouLpuL, mean arLerlal pressure also decreases. Cardlogenlc shock ls a
medlcal emergency.

():7%7; <"72 8)/#,*7
AcuLe myocardlal lnfarcLlon (mosL common cause)
Cardlac Lemponade
1enslon pneumoLhorax
ArrhyLhmlas (venLrlcular Lachycardla)
Masslve pulmonary embollsm

=)#1,>1?7",$,-?
($"."/)$ 7?@>#,@7 ).+ 7"-.7
"#$%&'$()
PypoLenslon -8lood pressure can fall up Lo 80/60
Cllgurla
1achycardla
AlLered menLal sLaLus

"*+,()
Skln appears pale and cold.
!ugular venous dlsLenslon ls found
ulmonary congesLlon or edema ls presenL.

9")-.,7"7
LkC: 1o see Lhe presence of elevaLed S1 segmenLs, lndlcaLlng myocardlal lnfarcLlon (Ml)
Lcho Lo check cardlac Lemponade
ChesL x-ray Lo deLecL Lhe presence of Lenslon pneumoLhorax
Pemodynamlc monlLorlng:
Swan-Canz caLheLer ls used Lo monlLor blood flow and hearL's funcLlon. lL measures lefL aLrlal
pressure by measurlng caplllary pulmonary wedge pressure.
!*%)#@%.#
1he lnlLlal managemenL ls malnLalnlng of
Alrway
8reaLhlng
ClrculaLlon

AfLerwards followlng LreaLmenL ls sLarLed dependlng upon Lhe cause.

ln case of myocardlal lnfarcLlon Lhe followlng LreaLmenL ls glven.
! Cxygen
! 8eLa blocker
! Morphlne
! Ace lnhlblLors
! nlLroglycerln
! nC lnLubaLlon
! SLaLln
! 1lssue plasmlnogen acLlvaLor (1A)
! CA8C
! AngloplasLy

lor cardlac Lemponade perlcarlocenLhesls ls performed.
1horacoLomy ls carrled ouL for Lenslon pneumoLhorax
1he drug such as amlodarone ls glven for cardlac arrhyLhmlas.
Low molecular welghL heparln ls glven Lo manage pulmonary embollsm.

vasopressors are also glven ln cardlogenlc shock. 1hey Lend Lo lncrease afLer and preload and
Lhus lncrease Lhe reduced blood pressure. 1hese are:
! uopamlne: lL lncreases Lhe renal flow and renal perfuslon
! uobuLamlne: lL lncreases Lhe cardlac ouLpuL
! noreplnephrlne or phenoleplnephrlne: lL ls used when boLh dopamlne and dubuLamlne do
noL help Lo ralse Lhe 8. noreplnephrlne lncreases conLracLlllLy, cardlac ouLpuL and
evenLually Lhe blood pressure.

uon'L glve lv (lnLravenous) flulds here slnce Lhey are harmful for Lhe paLlenL wlLh cardlogenlc
shock. LefL venLrlcular pressure ls already elevaLed so lv fluld should be avolded.

A.#*) ),*#"/ 4)$$,,. >:@> BACD=E
lnLra aorLlc balloon pump (lA8) ls someLlmes used Lo boosL myocardlal oxygen perfuslon.
8alloon ls placed ln aorLa. uurlng sysLole Lhls balloon deflaLes whlle durlng dlasLole lL lnflaLes.
8y dolng so lL lncreases afLerload and cardlac ouLpuL and consequenLly Lhe perfuslon and
oxygen Lo Lhe coronary arLery also lncreases and myocardlac oxygen demand decreases.

F:"GG%7
1. A paLlenL presenLs wlLh chesL paln, dlfflculL breaLhlng and confuslon afLer long Lrlp ln an
alrplane. Pls 8 was 80/40mmPg. Pls skln ls cold. !ugular veln ls dlsLended. 8ased on Lhe
flndlngs and hlsLory whaL ls Lhe llkely compllcaLlon of pulmonary embollsm ln Lhls paLlenL?
A. Pypovolemlc shock
8. Cardlogenlc shock
C. AnaphylacLlc shock
u. neurogenlc shock

1he correcL answer ls 8.
1he mosL llkely compllcaLlon pulmonary embollsm ln Lhls paLlenL ls cardlogenlc shock. 1hls ls
because masslve pulmonary embollsm leads Lo Lhe developmenL of cardlogenlc shock. lL ls also
apparenL from Lhe condlLlon of Lhe paLlenL. Pe has developed hypoLenslon, skln ls cold and hls
[ugular veln ls also dlsLended, polnLlng Loward cardlogenlc shock.

Pypovolemlc shock may presenL wlL hypoLenslon, cold skln buL Lhere ls no chesL paln unless
Lhere ls a Lrauma Lhere. Also, ln Lhls shock hemorrhage or bleedlng occurs. !ugular veln ls noL
dlsLended. 1he mosL lmporLanL ls LhaL pulmonary embollsm does noL lead Lo hypovolemlc
shock as no blood loss occurs here.

AnaphylacLlc shock ls Lhe characLerlsLlc of severe allerglc reacLlon. 1here may be a number of
slgns and sympLoms such as lLch, swelllng, rash, low 8, reduce hearL raLe, dyspnea, eLc. lL ls
noL Lhe compllcaLlon of pulmonary embollsm.

neurogenlc shock ls agaln noL Lhe compllcaLlon of pulmonary embollsm. lL occurs afLer splnal
cord ln[ury.

2. ln a paLlenL wlLh dlagnosls of myocardlal lnfarcLlon and cardlogenlc shock, whaL wlll be Lhe
mosL lmporLanL LreaLmenL of cholce?

A. lnLra aorLlc balloon pump (lA8)
8. AngloplasLy
C. CA8C
u. erlcarlocenLhesls

1he correcL answer ls A.
lnLra aorLlc balloon pump (lA8) ls Lhe mosL effecLlve and lmporLanL LreaLmenL of cholce ln
paLlenL wlLh myocardlal lnfarcLlon and cardlogenlc shock. 1hls ls because lL lncreases Lhe
perfuslon Lo Lhe myocardlum by lncreaslng Lhe coronary blood flow as well as slmulLaneously
decreases Lhe myocardlum oxygen demand, whlch ls lmporLanL Lo prevenL re-lnfarcL and Llssue
deaLh.

AngloplasLy can be used buL lL ls merely used Lo open up Lhe obsLrucLed vessels.

Coronary arLery bypass grafLlng (CA8C) ls baslcally a surglcal procedure LhaL ls performed Lo
lmprove Lhe blood flow. lL ls performed when Lhere ls severe coronary hearL dlsease (CPu).

3. erlcarlocenLhesls ls noL performed here and ls malnly done ln case of cardlac Lemponade.
A paLlenL presenLs wlLh cardlogenlc shock and myocardlal lnfracLlon. AfLer resusclLaLlon all of
Lhe followlng should be admlnlsLered based excepL?

A. 8eLa blocker
8. lv flulds
C. 1lssue plasmlnogen acLlvaLor (1A)
u. Morphlne

lv flulds should noL be admlnlsLered ln Lhe paLlenL wlLh cardlogenlc shock. 1hls ls because Lhey
are harmful for Lhe paLlenL wlLh cardlogenlc shock. 1hey can ralse Lhe volume and evenLually
lefL venLrlcular pressure whlch ls already elevaLed so lv fluld should be avolded.

8eLa blockers are useful ln paLlenL wlLh cardlogenlc shock and myocardlal lnfarcLlon because
Lhey reduce Lhe slze of lnfarcL as well as early morLallLy when admlnlsLered early. 8eLa blockers
also decrease Lhe lncldence of developmenL of recurrenL lschemla, venLrlcular arrhyLhmlas, or
relnfarcLlon.

1lssue plasmlnogen acLlvaLor (1A) can be glven ln paLlenL wlLh cardlogenlc shock and
myocardlal lnfarcLlon. lL helps Lo breakdown Lhe Lhrombosls.

Morphlne ls also used ln myocardlal lnfarcLlon as lL reduces Lhe paln.

4. A 18-year-old paLlenL ls admlLLed Lo Lhe hosplLal because he presenLs wlLh confuslon, chesL
paln, and confuslon and shorLness of breaLh afLer a blunL ln[ury ln Lhe chesL. Cn
examlnaLlon he ls pale wlLh cold clammy skln. Pls 8 ls 80/60 mmPg. Pls [ugular veln ls
dlsLended and urlnary ouLpuL noLed ls 17ml/hour. A dlagnosls of cardlogenlc shock ls made.
WhaL ls Lhe llkely cause of cardlogenlc shock ln Lhls paLlenL?

A. AcuLe myocardlal lnfarcLlon
8. ArrhyLhmlas
C. 1enslon pneumoLhorax
u. Masslve pulmonary embollsm

1he correcL answer ls C.
PlsLory of blunL Lrauma wlLh chesL paln and shorLness of breaLh ls Lhe Lyplcal sympLoms of
Lenslon pneumoLhorax. lL ls Lhe resulL of peneLraLlng ln[ury of Lhe lung causlng developmenL of
one-way valve. 1enslon pneumoLhorax can furLher cause Lhe developmenL of cardlogenlc
shock, Lhus lL ls Lhe mosL llkely cause here.

AcuLe myocardlal lnfarcLlon does noL occur afLer Lrauma. Also, lLs sympLoms are dlfferenL such
as here a person develops chesL paln LhaL radlaLes Lowards neck and lefL arm, sweaLlng,
palplLaLlon, eLc.

ArrhyLhmlas are Lhe condlLlon ln whlch hearL beaL ls lrregular. lL ls elLher Loo fasL or Loo slow. lL
ls presenLed wlLh shorLness of breaLh and also does noL develop afLer Lrauma.

Masslve pulmonary embollsm cannoL be Lhe llkely cause of cardlogenlc shock here because lL
does noL develop followlng a Lrauma. lor lL Lo develop, Lhere should be a hlsLory of prolong bed
resL, deep venous Lhrombosls, a long Lrlp ln a car or aero plane, eLc.

!"#$%& ()*+,#*#")- ./ 0)+#*

.12%,#"3%4 /)+ $%*+-"-5& ueflnlLlon, ClasslflcaLlon of CoarcLaLlon of AorLa, Cllnlcal SympLoms and
Slgns

6%/"-"#")-&
lL ls Lhe sLenosls or narrowlng of Lhe aorLa.

($*44"/",*#")- )/ ()*+,#*#")- ./ 0)+#*
re-ducLual
osL ducLual

1he mosL lmporLanL ducL ls Lhe ducLus arLerlosum. lL ls a llLLle plpe LhaL connecLs Lhe aorLa and
Lhe pulmonary arLery durlng lnLrauLerlne llfe. 1he ducLus arLerlosum laLer becomes llgamenLum
arLerlosum. lf someLhlng happens before, lL ls called preducLual coarcLaLlon.
lf someLhlng happens afLer, posL

reducLal coarcLaLlon only occurs ln lnfanLs.
1he adulL Lype ls Lhe posL ducLual coarcLaLlon. 8y deflnlLlon Lhls ls a sLenosls of Lhe aorLa pasL
Lhe llgamenLum arLerlosum or sLenosls dlsLal Lo Lhe ducLus arLerlosus ls known as posL ducLual
coarcLaLlon.

CoarcLaLlon of aorLa ls assoclaLed wlLh 1urner syndrome. AorLlc regurglLaLlon evenLually
develops. 1he murmur of coarcLaLlon of aorLa ls Lhe blowlng hlgh plLched dlasLollc murmur.

(*74%48 9"4: /*,#)+4&

;*#<)=<>4")$)5>

($"-",*$ 4>?=#)?4 *-@ 4"5-4
Low blood pressure ln lower exLremlLles (hypoLenslon)
Plgh blood pressure ln upper exLremlLles (hyperLenslon)
noLchlng of Lhe rlbs and pleural effuslon on chesL x-rays may be presenL.
oor growLh

6"*5-)4"4

!+%*#?%-#

!"#$%$&" ()#" *$(+,"

"#$%&' ()*+%#,-$#)./ )0 1,2$& 34),-56#-% 7.0-5,$#).

89:&,$#;&/ 0)5 %&-5.#.<' Iuentifying acute anu chionic complications of acute
myocaiuial infaiction.

=> (?5).#, @&-5$ A-#%25&
The main symptom is shoitness of bieath
Theiapy:
o ACE inhibitoi to ueciease bloou piessuie
o Biuietics (fuiosemiue) to eliminate fluiu
It can piogiess to caiuiogenic shock

B> 155?4$?*#-/
Piematuie ventiiculai Complexes (PvCs)
Atiial Fibiilation
ventiiculai tachycaiuia
o Theiapy:
! Amjouaion
! Electiical caiuioveision (if hemouynamically unstable)
ventiiculai fibiillation
o Theiapy
! 0nsynchionizeu uefibiillation
Paioxysmal Supiaventiiculai Tachycaiuia (PSvT)
Sinus tachycaiuia
Sinus biauycaiuia (atiopine if they aie uynamically unstable)
Asystole
Av block (pacemakei is neeueu if theie is IIb oi III uegiee Av block)

C> D&#.0-5,$#).
New ST elevation
o Check CK-NB level

E> D2+$25&
0ccuis uue to scai tissue foiming 1u uays aftei myocaiuial infaiction
Types:
o Fiee wall iuptuie (caiuiac tamponaue) - peiicaiuiocentesis is neeueu
o Inteiventiiculai wall iuptuie - suigeiy is neeueu
o Papillaiy muscles iuptuie (mitial ieguigitation) - mitial valve
ieplacement is neeueu
o ventiiculai aneuiysm

F> G&5#,-56#$#/
Inflammation of peiicaiuium
Biesslei's synuiome can uevelop weeks to months aftei myocaiuial
infaiction
Tieatment:
o Aspiiin

H> I&.$5#,2%-5 &*9)%#/*
Can cause stioke

!"#$%& ()*+%*"#,$ -%,.# /"0%,0%0
123%4#"5%0 6). $%,.*"*+& !"#$% '( )*+% ,$-.%/ )*+% '( !"#$% ,$-.% 0.1
20%$(3$45"(6(#47
/%6"*"#")*&

1) 8lghL Lo lefL shunL - lL means early cyanosls, blue bables
2) LefL Lo rlghL shunL - laLe onseL cyanosls also known as blue klds
"#$%& &' ()*& +%,-& '..,/+ #-
1eLralogy of lalloL (1Cl)
1ransposlLlon of greaL vessels
erslsLenL Lruncus arLerlosus
1rlcuspld aLresla
1oLal anomalous pulmonary venous reLurn
0)*& &' /#$%& +%,-&
! venLrlcular sepLal defecL (vSu)-Lhe mosL common congenlLal cardlac defecL.
! ALrlal sepLal defecL (ASu)
! aLenL ducLus arLerlosus (uA)
7,#8)98:0")$)+:
1he normal pressure lnslde Lhe rlghL aLrlum (8A) ls less Lhan 3 mmPg
1he normal pressure of Lhe rlghL venLrlcle (8v) ls 23/3mmPg, ln Lhe lefL aLrlum (LA) ls less Lhan
12 mmPg, ln Lhe Lv ls 130/10 and ln Lhe aorLa ls 130/90 mmPg.
1he pressure ln Lhe 8A ls less Lhan 3mmPg because Lhls allows blood Lo go lnLo Lhe hearL durlng
preload because pressure ln Lhe velns has Lo overcome Lhe pressure ln Lhe aLrlum. 1he pressure
ln Lhe 8v ls 23 mmPg, so Lo recelve blood, pressure ln lL would be equal or less Lhan Lhe
pressure ln Lhe 8A durlng dlasLole so LhaL blood can easlly flow lnLo Lhe rlghL venLrlcle. lL
means when hearL conLracLs Lhe pressure Lhe sysLole pressure whlch e[ecLs blood lnLo Lhe
pulmonary arLery has Lo be as hlgh as 23mmPg so LhaL lL can geL blood lnLo Lhe pulmonary
arLery. Also, blood from pulmonary arLery enLers lnLo Lhe lefL aLrlum. 1he sysLollc pressure
lnslde Lhe pulmonary arLery ls 23 and ln Lhe lefL aLrlum ls less Lhan 12, mean hlgh pressure Lo
low pressure.
1he sysLollc e[ecLlon pressure of 130/10 ln Lhe Lv pushes ouL Lhe blood lnLo Lhe aorLa.
lnlLlally, blood moves from hlgher pressure Lo lower pressure, l.e. lL shunLs from Lv Lo 8v. 8uL
Lhere ls sLlll a blood Lo enLer lnLo Lhe sysLemlc clrculaLlon. Cver Llme, Lhe wall of Lhe 8v geLs
Lhlck and Lhlcker Lhe wall Lhe hlgher Lhe dlasLollc pressure. CverLlme, pressure ln Lhe 8v
overcomes Lhe pressure ln Lhe Lv, now we geL deoxygenaLed blood lnLo Lhe 8v. 1haL's why lL
Lakes Llme and chlldren are called blue klds and a paLlenL ls sald Lo develop laLe onseL cyanosls.
Slmllar happens when blood shunLs from LA Lo 8A and paLlenL develops laLe onseL cyanosls.
Same ls wlLh Lhe uA, an open space beLween Lhe aorLa and Lhe pulmonary arLery.

($"*"4,$ 0:;9#);0 ,*< 0"+*0

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"#$%&' ()*+&,$#-& .&/0$ 1/#%20&

345&6$#-&, 7)0 %&/0*#*+' 0nueistanuing the pathophysiology of uiffeient types of
heait failuie, as well as iisk factois, clinical featuies, uiagnostics, anu tieatment
options.

8&7#*#$#)*'
Beait failuie is a synuiome which appeais when heait is not able to maintain
ciiculation anu to pioviue auequate peifusion to the iest of the bouy.

(/2,&,9 :#,; 7/6$)0,'
! Bypeitension
! Excess salt in intake

</$=)>=?,#)%)+?'
! Noimally, heait ieceives the bloou fiom the venous siue of the bouy, thiough the
supeiioi anu infeiioi vena cava (pieloau). Aftei the bloou enteis the iight atiium
anu then iight ventiicle, the heait muscle stietches, which is the stimulus foi the
contiaction. That way, the bloou is being pusheu fiom the ventiicles, which is
calleu stioke volume. Fiank - Stailing ielationship says that if the pieloau is
incieaseu, the contiactility incieases too, thus causing incieaseu stioke volume
anu consequently incieaseu caiuiac output.
! Becieaseu caiuiac output causes the activation of compensatoiy mechanisms,
incluuing caiotiu sinus baioieceptois, which in tuin incieases sympathetic
activity (incieaseu heait iate, contiactility, incieaseu pieloau anu afteiloau).
Anothei, slowei compensatoiy mechanism incluues iennin-angiotensin-
aluosteione system (watei anu souium ietention).
! The cause of heait failuie can be eithei systolic oi uiastolic uysfunction.
o Systolic uysfunction is causeu by loweieu contiactility of some paits of
heait muscle uue to myocaiuial infaiction, uilateu caiuiomyopathy,
myocaiuitis.
o Biastolic uysfunction appeais uue to impaiieu ielaxation of heait muscle.
The common causes aie hypeitiophic ventiiculai failuie (uue to
hypeitension, aoitic stenosis, aoitic ieguigitation, anu mitial stenosis)
anu iestiictive caiuiomyopathy (amyloiuosis, saicoiuosis,
hemochiomatosis).

(%#*#6/% ,?@>$)@, /*A ,#+*,
! Shoitness of bieath - Byspnea (because of pulmonaiy congestion)
! 0ithopnea - bieathing uifficulties when lying on the back
! Paioxysmal noctuinal uyspnea
! Noctuinal cough
! Biaphoiesis
! Colu extiemities
Specific signs of left-siueu heait failuie incluue:
! Caiuiomegaly
! SS gallop
! S4
! Ciackles (iales) in the lungs
! Bullness to peicussion of the lungs
Specific signs of iight-siueu heait failuie incluue:
! }ugulai venous uistension (}vB)
! Livei congestion anu hepatomegaly
! Ascites
! Peiipheial euema
! Right ventiiculai heaves
! Noctuiia
8#/+*),#,
! Chest X-Ray - caiuiomegaly, Keiley B-lines, inteistitial maikings, pleuial
effusion (blunting of the costophienic angle)
! Echocaiuiogiam is the most impoitant examination to make, because it
shows whethei the systolic ejection fiaction is loweieu.
! ECu finuings aie not specific.
"0&/$@&*$
1. Biet iestiiction (less than 4g of saltuay)
2. Biuietics
o Fuiosemiue - fiist line tieatment
o Thiaziue - seconu line tieatment
o Spiionolactone (can cause hypeikalemia!)
S. ACE inhibitois ueciease moitality in patients with heait failuie by uecieasing
pieloau anu afteiloau. Siue effects of ACE inhibitois aie: angioeuema, cough,
anu elevateu potassium levels. ACE inhibitois can be ieplaceu with saitans
(angiotensin ieceptoi blockeis) in patients with seiious cough.
4. Beta blockeis (Caiveuilol) aie shown to slow the piogiession of heait failuie
anu ueciease moitality.
S. uioup Iv patients (the teiminal stauium of heait failuie) shoulu ieceive
Bigitalis in oiuei to impiove caiuiac output. Byuialazine anu isosoibiu
nitiate can also be useu to iegulate the bloou piessuie in these patients.

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324&5$#6&. 7,0 %&80+#+9' 0nueistanuing the causes, iisk factois, pathophysiology,
uiagnosis, complications, anu tieatment of ueep venous thiombosis.

(&7#+#$#,+'
Beep venous thiombosis is the piesence of clots in ueep veins of legs.

:8-.&.; <#.= 785$,0.'
viichow's tiiau
o Enuothelial uamage
o Bypeicoagulability
o Stasis
Risk factois:
Congestive heait failuie (CBF)
Immobilization
0besity
Estiogen (use of biith contiol pills oi piegnancy)
Family histoiy of BvT
vaiicose veins
>8$/,)/?.#,%,9?'
0nlike aiteiial bloou vessels, bloou flow in veins uepenus only on muscle
contiaction. 0ne way valves enable biinging the bloou up towaius the heait.
Enuothelial uamage can be causeu by:
suigeiy
stasis (piolongeu iest oi tiavel)
malignancies
age.
Some heieuitaiy uiseases can cause hypeicoagulability.
Factoi v Leiuen ueficiency - leaus to incieaseu clotting
Piotein C anu S ueficiency
Antithiombin III ueficiency
BvT most often comes fiom iliac anu femoial veins.

:%#+#58% .?1)$,1. 8+@ .#9+.
Signs anu symptoms aie veiy vaiiable fiom patient to patient. Classic finuings
incluue:
Lowei extiemity pain anu swelling (especially while walking) - non-specific,
non-sensitive
Boman's sign - calf pain with uoisiflexion
Fevei

(#89+,.#.
0iuei Bopplei ultiasounu of the lowei extiemities to ueteimine
compiessibility of the veins. It is highly specific anu highly sensitive foi the
uetection of bloou clots in pioximal paits of extiemities, but not in the calf.
The most accuiate test is venogiaphy.
B - Bimei (veiy specific but only about Su% sensitive)

:,1)%#58$#,+.
Pulmonaiy embolism - uetacheu clots fiom ueep veins of lowei extiemities
tiavel thiough the infeiioi vena cava to the heait anu aie then towaius the
lungs. The iesult is pulmonaiy embolism.
! Big sauule emboli that obstiuct pulmonaiy aiteiy cause iight
ventiiculai failuie anu aiihythmia anu hypoxia.
Postthiombotic synuiome appeais uue to insufficiency of venous valve
system anu the inciease in hyuiostatic piessuie in venous capillaiies.
Phlegma ceiulea uolens - seveie leg euema iesulting in ischemia which
causes loss of sensitive anu motoi neuial function.

"0&8$1&+$
Anticoagulant tieatment is the most impoitant
! Bepaiin (piolongs PTT)
! vaifaiin (inhibits vitamin K)
! TPA (Tissue Plasminogen Activatoi)
INR shoulu be maintaineu between 2 anu S foi S-6 months.
uieenfielu filtei is useu to pievent pulmonaiy embolism
Suigeiy post-management (leg elevation, compiession stockings, eaily
ambulation, pneumatic compiession boots.
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/,0%1#"2%3 4-) $%*).".5& ueflnlLlon, Causes, aLhophyslology, Cllnlcal sympLoms and slgns,
ulagnosls and 1reaLmenL.

6%4"."#"-.&
lL ls Lhe flbrlllaLlon or qulckerlng of Lhe aLrlum.

7*83%39 :"3; 4*1#-)3&
ulmonary embollsm, CCu
laLrogenlc
8heumaLlc hearL dlsease / MlLral regurglLaLlon
ArLhrosclerosls
1hyrold (PyperLhyroldlsm, LhyroLoxlcosls)
LndocardlLls
Slck slnus syndrome

<*#=->=?3"-$-5?
normally, SA nodes flres and causes depolarlzaLlon of Lhe muscles. When aLrlum depolarlzes an
aLrlal conLracLlon occurs. ALrlum also squeezes aL Lhe same Llme, causlng blood Lo enLer lnLo
Lhe venLrlcles.
8uL ln case of aLrlal flbrlllaLlon, mulLlple dlfferenL ecLoplc nodes sLarL flrlng. noL only aLrlum
conLracLs, buL blood sLasls also occurs.

7$"."1*$ 3?@>#-@3 *.A 3"5.3
LlghLheadedness
Syncope
lasL hearL beaL
PyperLenslon

6"*5.-3"3
Cn LkC havlng aLrlal flbrlllaLlon, check
8aLe
8egular or lrregular C8S complex
waves
:C8S raLlo
8 lnLerval
C8S wldLh

ln aLrlal flbrlllaLlon, Lhere are no waves presenL. 1he paLlenL hearL raLe ls very varlable. 1he
hearL beaL ls lrregularly lrregular. no : C8S raLlo slnce no waves are presenL. 1he normal 8
lnLerval ls less Lhan 0.02 seconds buL ln aLrlal flbrlllaLlon, no waves are presenL so 8 lnLerval
cannoL be deLermlned. C8S complex ls usually of 120 mllllseconds. ln aLrlal flbrlllaLlon C8S
wldLh ls less Lhan 120 mllllseconds or normal.

!)%*#@%.#
aLlenLs are glven:
AnLlcoagulanLs such as warfarln (because of blood sLasls and lf anLlcoagulanLs are noL glven
paLlenLs wlLh Al can develop sLroke, mesenLerlc lschemla, claudlcaLlon, myocardlal
lnfracLlons, eLc.)
8eLa blockers such as meLhoprolol: 1hese help Lo decrease Lhe hearL raLe.
Calclum channel blockers e.g. nefldlplne: 1hey slow down Lhe hearL raLe.
ulgoxln: lL has a parasympaLheLlc effecL, sLlmulaLlng Lhe vagal nerves whlch slow down Lhe
flrlng from SA and Av node and Lhus allows decreaslng Lhe hearL raLe.

!"#$%& (%#)$ *%+ ,%$$ -./+01#"/2

Cb[ecLlves for learnlng: 1ypes of Pemoglobln and Crgan responslble for 8lood formaLlon durlng
lnLrauLerlne llfe.

leLal hemoglobln o2y2
AdulL hemoglobln o2
2

3%%45
llrsL Lhree Lo Len weeks: ?olk sac ls responslble for maklng blood.
6 weeks: Llver ls responslble for eryLhropolses.
13 and 30 weeks: Spleen Lakes on Lhls responslblllLy.
22 weeks Lo adulL: 8ones becomes responslble.

60"7
1. Whlch organ ls responslble for formaLlon of blood durlng 6 week of lnLrauLerlne llfe?
A. Spleen
8. 8ones
C. ?olk sac
u. Llver
1he correcL answer ls u.
Llver ls responslble for eryLhropolses durlng 6 week of lnLrauLerlne llfe.
?olk sac ls responslble for maklng blood durlng flrsL 3 Lo 10
Lh
week of lnLrauLerlne llfe.
Spleen becomes responslble for eryLhropolses durlng 13 and 30 weeks of llfe.
8ones becomes responslble from 22 weeks Lo onward ln adulL llfe.

Whlch organ ls responslble for formaLlon of blood durlng 23 week of lnLrauLerlne llfe?
A. Spleen
8. 8ones
C. ?olk sac
u. Llver
Lh

uurlng whlch sLage does Lhe yolk sac Lake parL ln eryLhropolses?
A. uoes noL Lake parL
8. 4
Lh
week
C. 22 week
u. 13
Lh
week
Lh
week of lnLrauLerlne llfe. So,
correcL opLlon ls 4
Lh
week here.
?olk sac does Lake parL ln Lhe formaLlon of blood durlng lnLrauLerlne llfe.
uurlng 13 and 30 weeks of llfe spleen becomes responslble for eryLhropolses.

4. WhaL ls Lhe dlfference beLween leLal hemoglobln and AdulL hemoglobln wlLh regard Lo Lhelr
sLrucLure?
A. leLal hemoglobln has Lwo alpha and Lwo beLa chalns.
8. AdulL hemoglobln has Lwo alpha and Lwo gamma chalns.
C. leLal hemoglobln has Lwo alpha and Lwo gamma chalns.
u. 8oLh are same and have no dlfference.

leLal hemoglobln has Lwo alpha and Lwo gamma chalns whlle adulL has Lwo alpha and Lwo beLa
chalns.

leLal hemoglobln has noL Lwo alpha and Lwo beLa chalns buL has Lwo alpha and Lwo gamma
chalns.

AdulL hemoglobln does noL have Lwo alpha and Lwo gamma chalns buL have has Lwo alpha and
Lwo gamma chalns.

leLal and adulL hemogloblns are noL same buL dlffer sLrucLurally as well as wlLh respecL Lo Lhelr
llfe.

3. Whlch organ ls responslble for formaLlon of blood durlng adulL llfe
A. Spleen
8. 8ones
C. ?olk sac
u. Llver
8ones are responslble for formaLlon of blood from 22 weeks Lo onward ln adulL llfe.
Lh

!"#$%& (%)*# +$,-./
012%-#"3%/ 4,* 5%)*6"67& ALrlo venLrlcular nodal block, 1ypes, llrsL degree Av block, Second
degree Av block, and 1hlrd degree hearL block.
8#*", 9%6#*"-:$)* ;,<)$ +$,-.
ln Av nodal block Lhere ls an lmpalrmenL of Lhe conducLlon beLween Lhe aLrla and venLrlcles of
Lhe hearL. SA node flres buL Lhls dlscharge does noL go beyond Lhe aLrla Lo Lhe venLrlcles.
!=>%/
1here are Lhree Lypes of blocks.
!" #$%&' )*+%** ,- ./0123
lL ls always prolonged ln case of flrsL degree Av block. normally, lL ls less Lhan 200 mlll seconds.
8uL ln flrsL degree Av block, Lhe 8 lnLerval ls greaLer Lhan 200 mlll seconds (greaLer Lhan 3
boxes). 1hls ls because Lhere ls a block causlng a delay ln Lhe conducLlon beLween Lhe Av node
down lnLo Lhe venLrlcle. lL ls a begln condlLlon and requlres no LreaLmenL.
4" 5*106) )*+%** ,- ./012
lL ls of Lwo Lypes
70.$'8 '9:* !3 lL ls also known as Wenckebach. A prolonged 8 lnLerval unLll a p wave falls Lo
conducL ls known as moblLz Lype 1. lL ls agaln a begln condlLlon and requlres no LreaLmenL.
70.$'8 '9:* 43 waves here fall Lo conducL buL Lhe 8 lnLerval ls consLanL. Pere Av node ls
conducLlng and Lhe block ls acLually ln Lhe bundle of Pls. lor Lhls reason, consLanL 8 lnLerval
appears. aLlenLs may have palplLaLlons. 1hey need pace maker lmplanLaLlon. 1hls Lype of
condlLlon can progress lnLo compleLe hearL block.
;" <=$%) )*+%** =*>%' ./012
lL ls Lhe absence of conducLlon of aLrlal lmpulses Lo Lhe venLrlcles whlch means Lhere ls no
correspondence beLween waves and C8S complexes. 1he aLrlal conducLlon ls dolng
everyLhlng lndependenLly. 1here ls a compleLe Av block. 1here ls dlssoclaLlon beLween aLrlal
lmpulses and venLrlcular conducLlon. CompleLe hearL block leads Lo asysLole. aLlenLs suffer
from presyncope eplsodes. 1hey develop llghLheadedness or dlzzlness. 1hey also develop
venLrlcular Lachycardla and aLrlal flbrlllaLlon. ln LkC, aLrlo-venLrlcular raLes are dlfferenL from
each oLher. waves are presenL. : C8S raLlo ls varlable. C8S wldLh ls normal. A pace maker ls
needed Lo LreaL Lhlrd degree Av block.
!"#$%& (%)*# +,-./0 1)0"20

1here are four hearL valves
AorLlc valve (rlghL upper sLernal border)
ulmonary valve
1rlcuspld valve (lefL lower sLernal border)
MlLral valve

1he apex ls ln Lhe 3
Lh
and 6
Lh
lnLercosLal space.
1he normal hearL sound ls S1 and S2
S1 ls Lhe sound heard when Lhe mlLral and Lhe Lrlcuspld valve close as Lhe blood flow from
aLrlum Lo Lhe venLrlcle and venLrlcle sLarLs Lo squeeze.
S2 hearL sound ls due Lo closure of aorLlc and pulmonary valve and ls heard as Lhe venLrlcular
sysLole ends and Lhe venLrlcular dlasLole beglns.
S3 sound ls presenL ln case of pregnancy or ln congesLed hearL fallure. lL can be heard ln Lhe
apex and ln Lhe Lrlcuspld area.
S4 sound ls due Lo Lhe aLrlum conLracLlng agalnsL a non-compllanL venLrlcle.

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345&2$#.&- 67+ %&8+,#,1' 0nueistanuing the basics of hypeitensive uigency anu
emeigency, anu leain to uiagnose them anu apply fast anu effective tieatment.

9&6#,#$#7,-'
Bypeitension is a meuical conuition in which bloou piessuie is highei than
14u9u mmBg in two sepaiate occasions.
Bypeitensive uigency - bloou piessuie of 22u12u mmBg oi highei without
any enu oigan uamage.
Bypeitensive emeigency - bloou piessuie of 22u12u mmBg oi highei with
enu oigan uamage.
Bypeitensive encephalopathy - bloou piessuie of 24u14u mmBg oi highei
with neuiologic symptoms.
Pieeclampsia - Bypeitensive episoues uuiing piegnancy (14u9ummBg oi
highei) with pioteinuiia anu euema of lowei extiemities.

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Risk factois:
Bypeitension is the most pievalent in Afiican Ameiicans
Nen aie moie often affecteu than women
Causes:
Noncompliance to meuications
Sympathomimetic uiugs
Cushing's synuiome
Eclampsia
Pheochiomocytoma
Bypeialuosteionism

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! Patient using can uevelop hypeitensive uigency uue to bau compliance to
antihypeitensive meuication they noimally use.
! Cocaine, LSB, anu phenylephiine useis can expeiience hypeitensive uigency
uue to sympathomimetic effects of these uiugs.
Incieaseu bloou piessuie uamages the enuothelium of bloou vessels. That causes
the ueposition of pioteins in the walls of the bloou vessels, thus causing basement
membiane thickening. That thickening naiiows the walls of bloou vessels causing
ischemia by uecieasing bloou flow thiough the bloou vessels.

:%#,#28% -)0*$70- 8,A -#1,-
Beau
o Beauaches
o Bluiiy vision (uue to papiloeuema)
o Alteieu mental status
o Weakness in aims oi legs, numbness, tingling, etc.
o Retinal hemoiihages
Chest
o Chest pain
o Shoitness of bieath
o Pulmonaiy ciacklesiales
o }ugulai venous uistension
o SS
Kiuneys
o Anuiia
o Bematuiia
o Incieaseu cieatinine
Legs
o Euema

9#81,7-#-
! It is necessaiy to take goou histoiy.
! Physical exam:
o If theie is alteieu mental status, iule out the othei possible causes in
oiuei to blame hypeitension.
o Full neuiological exam
o Funuoscopic exam
! Laboiatoiy techniques:
o ECu
o Electiolytes
o Cieatinine
o B0N
o WBC count
o LFTs
o Pioteins anu bloou in uiine
! Iamging:
o CT scan of the heau
o Chest X-Ray

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The aim is to ueciease the bloou piessuie by 2S% in fiist 1 - 2 houis.
*If patient's bloou piessuie is 24u14u mmBg, the piessuie aftei 1 - 2 houis shoulu
be 18u9u mm Bg.
Neuication:
Beta blockeis (contiainuicateu if the patient useu uiugs)
Souium nitiopiussiue
Fenoluopam
Byuialazine
Nitioglyceiin

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Cb[ecLlves for learnlng: ueflnlLlon, Causes, aLhophyslology, Slgns and SympLoms SLages of
hypovolemlc shock, ulagnosls and 1reaLmenL
2%3"4"#"+4&
Low blood volume leads Lo decrease cardlac ouLpuL.
5678%89 :"81 36.#+;8&
1. Pemorrhaglc

1rauma
Cl 8leed
8eLroperlLoneal bleed

2. non hemorrhaglc
8urns
vomlLlng
Masslve waLery dlarrhea
1hlrd space-- AsclLes ln masslve llver clrrhosls
Low albumln (hypoalbumlnemla)

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Low blood volume causes low cardlac ouLpuL. 1he parameLers of hypovolemlc shock lnclude
decreased cardlac ouLpuL, lncreased LoLal perlpheral reslsLance (18) and decreased pulmonary
wedge pressure.

5$"4".6$ /)-*#+-8 >4? /"=48
PypoLenslon
Cold, clammy skln
2"6=4+8"8
Cv (cenLral venous pressure)
ulmonary caplllary wedge pressure ls low.
SysLemlc vascular reslsLance ls hlgh.

/#6=%8 @3 ()*+,+$%-". /0+.1
/#6=% A& lL ls characLerlzed by 10 Lo 13 (<73ml) loss of blood. 1he normal cardlac ouLpuL ls
equal Lo 3L (3000ml) so all Lhe parameLers such as pulse, sysLemlc blood pressure, resplraLlon,
caplllary reflll, CnS dysfuncLlon and urlne ouLpuL are noL affecLed buL normal.

/#6=% B& Pere 20 Lo 30 (73 Lo 1300ml) blood ls losL. Pere sysLemlc 8 ls normal, buL pulse ls
lncreased and hearL raLe ls hlgh, whlle all oLher parameLers are decreased.

/#6=% C& Pere 30 Lo 40 (1300 Lo 3000 ml) blood loss occurs. Pere blood pressure decreases
severely, hearL raLe lncreases (due Lo reflex Lachycardla), pulse pressure and caplllary reflll boLh
decrease. LacLlc acldosls ensues. A paLlenL ls confused and hls urlnary ouLpuL becomes less Lhan
20ml/hour (paLlenL develops severe ollgurla and almosL golng Lo develop anurla).

/#6=% D& Pere greaLer Lhan 40 blood loss occurs (l.e. > 2000ml). 1he affecL person ls leLharglc.

!;%6#-%4#

MalnLaln alrways, breaLhlng and clrculaLlon. lor malnLalnlng alrways lncubaLe Lhe paLlenL.
Manual pressure over bleedlng ls lmporLanL Lo sLop bleedlng.
ass nC Lube Lo avold developmenL of asplraLlon pneumonla
lv flulds normal sallne.

E7"FF%8
1. A paLlenL presenLs wlLh confuslon and leLhargy. Pe susLalns a Lrauma on hls abdomen. Cn
examlnaLlon hls 8 ls 80/30. Pls skln ls cold and clammy. 1he [ugular venous pressure ls
normal. WhaL ls Lhe mosL llkely dlagnosls?
8. Cardlogenlc shock
C. AorLlc aneurysms
u. neurogenlc shock
1he correcL answer ls A
1he mosL llkely dlagnosls ls hypovolemlc shock. 1hls ls because paLlenL suffers from a Lrauma on
hls abdomen so lL may have cause reLroperlLoneal bleed. lor Lhls reason, hls 8 has fallen and
hls skln ls cold.
Slnce Lhere ls no complalnL of chesL paln, so Lhe cardlogenlc shock ls unllkely here. 1he [ugular
venous pressure musL be elevaLed ln case of cardlogenlc shock.
AorLlc aneurysm ls a condlLlon ln whlch aorLa ls dllaLed Lo greaLer Lhan 1.3 Llmes Lhan lLs normal
slze. 1he sympLoms of Lhls problem appear when aneurysm ls rupLured. 1here may be
abdomlnal and back paln. AorLlc aneurysm rupLure ls a serlous medlcal condlLlon.
neurogenlc shock resulLs when Lhere ls ln[ury Lo Lhe splnal cord, affecLlng Lhe sympaLheLlc
sysLem. Skln here ls warm. 8radycardla ls also presenL.

2. A paLlenL ls admlLLed ln Lhe hosplLal afLer a dlagnosls of hypovolemlc shock ls made. WhaL ls
Lhe mosL common cause of Lhls shock?
A. 8urns
8. ln[ury Lo splnal cord
C. lluld shlfL
u. 8lood loss
1he mosL common cause of hypovolemlc shock ls blood loss. Loss of blood leads Lo lmmedlaLe
volume depleLlon. 1hls depleLlon furLher affecLs cardlac ouLpuL whlch becomes reduced.
8urns may lead Lo developmenL of hypovolemlc shock buL ls noL as common as blood loss ls.
ln[ury Lo splnal cord ls Lhe mosL common cause of neurogenlc shock.
lluld shlfL can also cause hypovolemlc shock slnce lL leads Lo decrease ln blood pressure Lo
severe exLenL buL lL occurs rarely.

3. A paLlenL ls presenLs wlLh severe bleedlng and confuslon afLer a Lrauma. Pls 8 ls
80/40mmPg. Pls hearL raLe ls 120beaLs/mln. Pe ls admlLLed ln Lhe hosplLal and necessary
resusclLaLlon ls glven. lL ls however found LhaL hls urlnary ouLpuL ls 13ml/ hour. WhaL ls Lhe
mosL llkely sLage of hypovolemlc shock ln Lhls paLlenL?
A. SLage 1
8. SLage 2
C. SLage 3
u. SLage 4
1he mosL llkely sLage of hypovolemlc shock ln Lhls paLlenL based on hls cllnlcal presenLaLlon ls
sLage 3. ln Lhls sLage 30 Lo 40 blood loss occurs, leadlng Lo severely dropplng of blood
pressure and urlnary ouLpuL. PearL raLe however ls lncreased. A person develops lacLlc acldosls
and consequenLly alLered menLal sLaLus and confuslon. ln Lhls paLlenL urlne ouLpuL ls markedly
reduced.
ln case of SLage 1 person does noL have above menLloned sympLoms. Pe may be asympLomaLlc
because here only 10 Lo 13 blood loss has occurred.
SLage 2 ls characLerlzed by 20 Lo 30 loss of blood. Pere sysLemlc 8 ls normal, buL hearL raLe
ls hlgh.
SLage 4 ls a severe form of hypovolemlc shock characLerlzed by greaLer Lhan 40 blood loss. A
person may be unconsclous and anurlc.

Title: Infective Endocarditis

Objectives for learning: Definition, Causes, Classification, Complications Of Infective
Endocarditis, Clinical symptoms and signs, Diagnosis and Treatment

Definition:
Infection of the heart valve is called infective endocarditis.

Causes/ Risk factors:
Bacteria

Classification
1. Acute Endocarditis (less than 6 weeks): The culprit is staphylococcus aureus (more common
in IV drug abusers)
2. Subacute Endocarditis is caused by:
Streptococcus viridians, most prone to dentistry procedures
Enterococcus (bacteria arise from GI tract)

3. Native Valve Endocarditis
Streptococcus viridans
Haemophilus
Actinobacillus
Cardiobacterium
Ekenella
Kingella

4. Prosthetic Endocarditis
The bacteria responsible here are:
Staphylococcus epidermidis (60 days of surgery)
If more than 60 days then staphylococcus aureus is responsible

In blood cultures if streptococci bovi appears positive then it may probably be due to colon
cancer

Complications Of Infective Endocarditis
Cardiac failure
Glomerulonephritis
Mycotic abscess

Pathophysiology

Clinical Symptoms And Signs
Fever
Roth spots (retinal lesions due to vasculitis)
Oslers nodes (painful nodes in the pads of the finger or the toes due to vasculitis)
Murmur
Jane way lesions (lesions on the palm and the soles due to emboli)
Anemia
Nail bed hemorrhages/ Splinter hemorrhages
Emboli

Diagnosis
Blood culture
Transesophageal echocardiogram

Treatment
Empiric Treatment: Start with vancomycin and gentamycin and give intravenously before the
results of blood culture come.

Once the blood cultures come positive for particular organism, such as for streptococcus
viridians then give penicillin. But if a person is allergic to penicillin then switch to ceftriaxone
and gentamycin.

If person is IV drug abuser, then given antibiotic against staphlococcus aureus. Nafcilin for 4
weeks is given plus gentamycin for 5 days

In case of Methicillin-resistant Staphylococcus aureus (MRSA) give vancomycin for 6 weeks.

And if blood culture comes positive for enterococcal bacteria give penicillin/ampicillin (for 4 to
6 weeks)

If a person is allergic to penicillin then administer vancomycin + gentamycin (for 4 to 6 weeks).

Quiz

1. A 15-year-old patient presents with fever and joints pain for 3 day. A patient also complains
of night sweat. On examination she is pallor. Splinter hemorrhage and painful nodules on
the fingers pad are found. What is the most likely diagnosis?
A. Polymyalgia Rheumatica
B. Atrial Myxoma
C. Reactive Arthritis
D. Infective endocarditis
The correct answer is D.
The most likely diagnosis is infective endocarditis. It is characterized by low grade fever, Oslers
nodules, anemia and splinter hemorrhage. In addition, Jane way lesions and Roths spots are also
present. It is a condition of the inflammation of the valves of the heart.
Polymyalgia rheumatica (PMR) is basically a syndrome of unidentified etiology. It usually
occurs in adults and is characterized by muscle pain frequently of the shoulder girdles and the
hip. A patient usually complains of morning stiffness that lasts for more than one hour.
Atrial Myxoma is a tumor of the heart. It is a benign tumor. Fever, joint pain, shortness of breath
and weight loss occur. Painful nodules are not found here, so it is not a correct diagnosis.
Reactive arthritis is an autoimmune condition which is the result of an infection. It is
characterized by conjunctivitis, urethritis and arthritis. This is not correct as patient has no such
complaints.

2. Which of The following is not the cutaneous involvement of infective endocarditis?
A. Janeway's lesions
B. Skin petechiae
C. Roth's spots
D. Osler's Nodules
The correct answer is C.
Roth's spots are not the cutaneous involvement of infective endocarditis. These are basically the
retinal lesions due to vasculitis.
Skin petechiae are usually found in patient with infective endocarditis.
Janeway's lesions are one of the cutaneous involvements of infective endocarditis. These are
lesions on the palm and the soles and are due to emboli.
Osler's Nodules are again the cutaneous manifestation of this condition i.e. infective
endocarditis. These are painful nodes present in the pads of the finger or the toes due to
vasculitis.

3. A person with infective endocarditis has a history of using drugs for pleasure. Which
antibiotic is best for this patient?
A. Nafcilin
B. Vancomycin
C. Amoxacillin
D. Rifampicin
The correct answer is A.
Nafcilin is the drug of choice for the person who is a drug abuser and also suffered from
infective endocarditis.
Vancomycin is usually preferred for those who are allergic to penicillin.
Amoxacillin has no such role in case of infective endocarditis.
Likewise, rifampicin is not the drug used for patients with infective endocarditis.

4. Which of the following statements concerning infective endocarditis is not right?
A. Empiric treatment of infective endocarditis includes vancomycin and gentamycin
B. Splenomegaly is found to occur commonly in acute infective endocarditis than the sub
acute one.
C. Glomerulonephritis is one of the complications of infective endocarditis
D. Infective endocarditis takes place within 2 weeks of bacteremia
The correct answer is B.
The incorrect option regarding infective endocarditis is A. Splenomegaly is not commonly found
in case of acute infective endocarditis. It is rather present in sub acute infective endocarditis.
Empiric treatment of infective endocarditis includes vancomycin and gentamycin. This treatment
is generally started before the report of blood cultures come.
Clinical manifestations of this condition usually take place within 2 weeks of the provocative
bacteremia in approximately 80% of cases.
Glomerulonephritis is one of the complications of infective endocarditis.

5. All of the following are responsible for native valve endocarditis except

A. Streptococcus viridans
B. Streptococcus viridians
C. Haemophilus
D. Ekenella

The correct answer is B.
Streptococcus viridians do not cause native valve endocarditis instead infection by these bacteria
occurs following a dentistry procedure.

Streptococcus viridians are responsible for native valve endocarditis. 55-65% cases of all native
valve endocarditis are caused by viridans streptococci.

Haemophilus and Ekenella both are the cause behind native valve endocarditis.

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345&.$#6&2 7+* %&8*)#)9' Causes, iisk factois anu pathophysiology anu
complications of hypeitension.

:&7#)#$#+)' Bypeitension is high bloou piessuie (>14u9u). Essential hypeitension
is high bloou piessuie without iuentifieu cause (9S% of all patients). Seconuaiy
hypeitension has known causes (S% of patients).

;8-2&2< =#2> 78.$+*2'
Risk factois:
Age
uenuei (men have highei iisk than women)
Race (Afiican Ameiicans have highei iisk of hypeitension)
0besity
Seuentaiy lifestyle
Incieaseu souium intake (>4guay)
Alcohol

Causes:
Seconuaiy hypeitension
o Renal causes
! Renal aiteiy stenosis
! Chionic ienal failuie
! Polycystic kiuney uisease
o Enuociine system
! Bypeithyioiuism
! Bypeialuosteionism
! Bypeipaiathyioiuism
! Cushing synuiome
! Pheochiomocytoma
o Neuications
! 0ial contiaceptives
! Becongestives
! NSAIBs
! TCAs
o Coaictation of the aoita
o Illegal uiugs
! Cocaine
o Sleep apnea
o Biith contiol pills

?8$/+1/02#+%+90'
Becieaseu peifusion thiough the ienal aiteiy stimulates iennin-angiotensin-
aluosteione system, thus incieasing peiipheial vasculai iesistance anu bloou
piessuie.
Bypeithyioiuism incieases metabolic iate anu consequently the bloou
piessuie.
Bypeialuosteionism incieases souium ieabsoiption anu causes
hypeinatiemia, thus incieasing intiavasculai volume anu bloou piessuie.
Patients with Cushing synuiome have excess amount of coitisol which
activates auienal meuulla to piouuce moie noiepinephiine anu epinephiine,
thus incieasing bloou piessuie.
In pheochiomocytoma, high amounts of noiepinephiine anu epinephiine aie
piouuceu uue to tumoi of auienal meuulla.

Becongestives aie intenueu to make a local vasoconstiiction, but also have
impact on systemic bloou piessuie inciease.

NSAIBs block C0X2, thus blocking the synthesis of vasouilatatoiy
piostaglanuins.

Cocaine inhibits the ieuptake of noiepinephiine, thus incieasing its bloou
concentiation anu bloou piessuie.

Sleep apnea causes iespiiatoiy aciuosis which piovokes hypoxia. Bypoxia
leaus to hypoxic vasoconstiiction in the lungs which leaus to pulmonaiy
hypeitension anu eventually high bloou piessuie.

Incieaseu systemic vasculai iesistance incieases the afteiloau, so the heait has to
woik much haiuei, which leaus to left ventiiculai hypeitiophy. 0vei time, heait
function becomes weakei leauing towaius uilation of the heait anu heait failuie.

Bigh bloou piessuie acceleiates aiteiioscleiosis by uamaging enuothelium of bloou
vessels.

;+@1%#.8$#+)2
Caiuiac complications
o Coionaiy aiteiy uisease (myocaiuial infaiction)
o Left ventiiculai hypeitiophy anu heait failuie
o Stioke (hemoiihagic), TIAs, ischemic stioke
o Aoitic uissection
o Peiipheial aiteiial uisease
Eye changes
o Papilloeuema
o Retinal hemoiihages
Kiuneys
o Nephioscleiosis
o Renal failuie

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023%4#"5%6 789 $%:9;";<& ueflnlLlon, Causes/ 8lsk facLors, aLhophyslology, SympLoms, ulagnosls
and 1reaLmenL.

=%7";"#"8;&
8lood reLurns lnLo lefL slde of Lhe hearL lnLo Lhe lefL aLrlum from Lhe pulmonary veln rlghL back
lnLo lefL venLrlcle lnLo Lhe aorLa Lo Lhe resL of Lhe body.
When mlLral valve closes lL glves S1. 1he blood flows ouL Lhrough Lhe aorLa durlng sysLole and
durlng dlasLole mlLral valve opens up Lo allow blood Lo reLurn back Lo Lhe hearL buL aL Lhe same
Llme aorLlc valve and pulmonary valve boLh close and lL glves S2. uurlng sysLole boLh Lrlcuspld
and mlLral valve close Lo glve S1 sound.

uurlng sysLole mlLral valve blow up and so blood goes back Lo Lhe lefL aLrlum, lncreaslng Lhe
pressure lnslde lL, causlng decrease ln cardlac ouLpuL, hyperLenslon and cardlogenlc shock.

>:?6%6@ *"6A 7:4#896&
+4?#% 4:?6%6& LndocardlLls, S.aureus lnfecLlon, Myocardlal lnfarcLlon (rupLure of paplllary
muscles)
>B98;"4 >:?6%6& 8heumaLlc hearL dlsease, Marfan syndrome, and cardlomyopaLhy.

C:#B8DBE6"8$8<E
LA pressure lncreases here. 1he slze of lefL aLrlum ls normal buL blood now backs up, back Lo
Lhe pulmonary veln, pulmonary caplllarles, pulmonary edema, congesLlon and evenLually
pulmonary hyperLenslon.

>$";"4:$ 6EFD#8F6 :;G 6"<;6
! uyspnea
! alplLaLlons
! roxlmal nocLurnal dyspnea
! ulmonary edema

C-& PolosysLollc murmur

=":<;86"6
! ChesL x-ray shows dllaLed lefL venLrlcle and pulmonary edema
! Lcho show presence of M8, dllaLed lefL venLrlcle and decreased lefL venLrlcular funcLlon

!9%:#F%;#
(%G"4:$ #B%9:DE& lL ls sLarLed wlLh afLerload reducLlon medlcaLlons such as ACL lnhlblLors (such
as llslnoprll)
uecrease salL lnLake
ulgoxln
lor arrhyLhmlas glve CC8 (calclum channel blocker) Lo LreaL aLrlal flbrlllaLlon (Al)
AnLlcoagulaLlon Lherapy (paLlenL may have Al)
H?9<"4:$ !9%:#F%;#& aLlenL needs a mlLral valve replacemenL or mlLral valve repalr.

I?"J
1. A paLlenL presenLs wlLh complaln of aLLacks of severe shorLness of breaLh and coughlng aL
nlghL. 1he flrsL hearL sound appears sofL whlle Lhe apex beaL ls laLerally dlsplaced. 1here ls
a murmur appeared followlng flrsL hearL sound and ls of hlgh-plLched. ChesL x ray shows
enlargemenL of Lhe lefL aLrlum and Lhe lefL venLrlcle. WhaL ls Lhe mosL probable dlagnosls?
A. MlLral regurglLaLlon
8. MlLral sLenosls
C. 1rlcuspld regurglLaLlon
u. 1rlcuspld sLenosls
1he mosL probable dlagnosls ls MlLral regurglLaLlon. 1hls ls characLerlzed by Lhe posL nocLurnal
dyspnea, orLhopnea and palplLaLlons. PolosysLollc murmur appears followlng flrsL hearL sound
and ls of hlgh-plLched. ChesL x ray shows enlargemenL of Lhe lefL aLrlum and Lhe lefL venLrlcle.
MlLral sLenosls ls a condlLlon characLerlzed by Lhe narrowlng of Lhe mlLral valve orlflce. lL ls
presenLed wlLh Lhe same sympLoms as LhaL of mlLral regurglLaLlon. 1applng apex beaL ls presenL
wlLh very loud flrsL hearL sound. ChesL x ray shows lefL aLrlal enlargemenL.
1rlcuspld regurglLaLlon ls Lhe consequence of problem wlLhln Lhe Lrlcuspld valve. 1he sympLoms
lnclude Lhose of rlghL-slded hearL fallure, such as edema, asclLes, [ugular venous dlsLenslon
and hepaLomegaly. !ugular venous pressure ls found Lo be elevaLed. Lcho shows Lhe presence
of enlargemenL of rlghL venLrlcle and rlghL aLrlum.
1rlcuspld valve sLenosls ls a dlsease of Lhe valves of Lhe hearL whlch resulLs due Lo narrowlng of
Lhe Lrlcuspld valve orlflce. An abnormal pulse ls felL ln Lhe [ugular veln wlLhln Lhe neck durlng
a physlcal examlnaLlon.
2. When does Lhe mlLral regurglLaLlon Lake place?
A. uurlng sysLole
8. uurlng dlasLole
C. uurlng boLh sysLole and dlasLole
1he mlLral regurglLaLlon Lakes place durlng sysLole. uurlng sysLole mlLral valve belng abnormal
could noL propel blood Lo Lhe lefL venLrlcle and so blood goes back Lo Lhe lefL aLrlum, lncreaslng
Lhe pressure lnslde lL wlLh subsequenL consequences.
1he opLlon 8 and C are noL correcL slnce durlng dlasLole pressure exerLed on Lhe walls of Lhe
arLerles are noL enough Lo proper blood from lefL aLrlum Lo lefL venLrlcle.
3. A 46 year old man wlLh severe mlLral regurglLaLlon has no sympLoms. Pls lefL venLrlcular
e[ecLlon fracLlon ls approxlmaLely 43 whlle an end-sysLollc dlameLer lndex ls abouL 2.9
cm/m2. WhaL would be Lhe mosL sulLable LreaLmenL ln Lhls paLlenL?

A. no LreaLmenL
8. MlLral valve replacemenL or repalr
C. ACL lnhlblLor Lherapy
u. ulureLlc Lherapy and dlgoxln

1he correcL answer ls:8
A zurglcal LreaLmenL ls recommended ln case of severe mlLral regurglLaLlon even lf Lhe paLlenL
ls asympLomaLlc. 1hls ls because when Lhe lefL venLrlcular e[ecLlon fracLlon falls down below
60 lL may cause a progresslve dysfuncLlon of lefL venLrlcle.
lf no LreaLmenL ls glven paLlenL may develop cardlac fallure and even deaLh of Lhe person
ensues.
ACL lnhlblLor Lherapy ls of no value ln case of asympLomaLlc paLlenL. lL ls however used when
paLlenL wlLh mlLral regurglLaLlon develops hyperLenslon.
ulureLlc Lherapy and dlgoxln are lndlcaLed when Lhere ls presence of hyperLenslon and
arrhyLhmlas respecLlvely. Slnce Lhls paLlenL ls asympLomaLlc Lherefore boLh drugs are noL used
here.

4. WhaL ls Lhe Lype of murmur found ln mlLral regurglLaLlon (M8)?
A. ansysLollc murmur
8. resysLollc murmur
C. PolosysLollc murmur
u. PolodlasLollc murmur
1he correcL answer ls: C.
ln mlLral regurglLaLlon PolosysLollc murmur ls presenL. lL ls a hlgh-plLched murmur found aL Lhe
apex. lL sLarLs from Lhe end of S1 and remalns Llll Lhe beglnnlng of S2.
ansysLollc murmur ls alLhough found ln M8 buL lL ls also presenL ln oLher condlLlons of Lhe
hearL. lL sLarLs from Lhe beglnnlng of S1 and remalns Llll Lhe end of S2.
resysLollc murmur ls presenL ln case of mlLral sLenosls and appears beLween Lhe ! sound and
S1.
PolodlasLollc murmur beglns from Lhe end of S2 and remalns Llll Lhe beglnnlng of S1 and ls noL
presenL ln M8.
3. A 33 years old paLlenL presenLs wlLh dlfflculLy ln breaLhlng for one monLh. Pe also suffers
from apprehenslon. Pe gave a hlsLory of severe fever and formaLlon of leslons on Lhe hand
and flngers. A dlagnosls of mlLral regurglLaLlon was made based on Lhe cllnlcal examlnaLlon
and radlologlcal resulLs. WhaL ls Lhe llkely cause of mlLral regurglLaLlon ln Lhls paLlenL?
A. lnfecLlve endocardlLls
8. Myocardlal lnfarcLlon
C. 8heumaLlc hearL dlsease
u. Marfan syndrome
1he correcL answer ls: A.
AlLhough all Lhe opLlons can cause mlLral regurglLaLlon buL lf we see LhaL Lhls paLlenL glves
hlsLory of fever as well as leslons on hands and flnger (mlghL be 8oLh's spoLs or Csler's nodes),
lL ls Lhen lnfecLlve endocardlLls.
Myocardlal lnfarcLlon ls a serlous condlLlon presenLs wlLh chesL paln, dyspnea, sweaLlng and
palplLaLlon. 1herefore, Lhls ls noL correcL wlLh regard Lo Lhls paLlenL's scenarlo.
8heumaLlc hearL dlsease ls usually more common ln chlldren. lL noL only affecLs Lhe hearL, buL
also Lhe [olnLs and Lhe cenLral nervous sysLem. lL ls Lhe resulL of rheumaLlc fever caused by a
precedlng lnfecLlon by group A sLrepLococcal.
Marfan syndrome ls baslcally a geneLlc dlsorder whlch ls dlagnosed earller. 1hls syndrome Lends
Lo affecL Lhe skeleLal sysLem. eople wlLh Lhls dlsorder are abnormally Lall and have
long llmbs and flngers.
!"#$%& (%)*+,%-". /0+.1

234%.#"5%6 7+* $%8*-"-,& ueflnlLlon, Causes, aLhophyslology, arameLers of neurogenlc
Shock, Cllnlcal sympLoms and slgns and 1reaLmenL.
9%7"-"#"+-&
neurogenlc Shock ls deflned as Lhe absence of sympaLheLlc Lone leadlng Lo sysLemlc
vasodllaLaLlon. Powever, Lhere ls an unopposed vagal nerve acLlvlLy.
:8)6%6; <"61 78.#+*6&
Splnal cord ln[ury (lL causes loss of sympaLheLlc Lone and unopposed vagal acLlvlLy vagal nerve
Lone leads Lo hypoLenslon).
=8#0+>0?6"+$+,?
SysLemlc vasodllaLaLlon causes decrease ln sysLemlc vascular reslsLance and hypoLenslon
(80/40). 1he end resulL ls bradycardla wlLh hearL raLe of 20beaLs/mlnuLe.
=8*8@%#%*6 +7 (%)*+,%-". /0+.1
uecreased cardlac ouLpuL, decreased LoLal perlpheral reslsLance (18) and decreased
pulmonary caplllary wedge pressure.
:$"-".8$ 6?@>#+@6 8-A 6",-6
PypoLenslve
8radycardla as sympaLheLlc sysLem ls loss
Warm skln
urlne ouLpuL mlghL be low or normal
9"8,-+6"6
!*%8#@%-#
MalnLaln Alrway, breaLhlng and clrculaLlon (A8C)
Moblllze splne (cover on neck)
lv flulds ls Lhe malnsLay of Lherapy
Also sLarL domaplne slnce lL lmproves cardlac conLracLlllLy and Lhus Lhe perfuslon ls
enhanced.
AdmlnlsLer dobuLamlne Lo lncrease cardlac ouLpuL.
lor braydcardla glve aLroplne
lor neurodeflclL glve meLhylprednlsolone
1ry Lo malnLalnlng Lhelr body LemperaLure
Call neurosurgery deparLmenL, orLhopaedlcs and Lrauma surgeons

Culz
A paLlenL susLalns an ln[ury ln Lhe back. now he ls presenLed ln Lhe nlghL wlLh decrease urlnary
ouLpuL and leLhargy. Pe Lells LhaL he has urlnaLed once ln Lhe mornlng up Llll now. Pe has been
urlnaLlng Lwlce a day only for 2 days. Cn examlnaLlon hls LemperaLure ls 99l. 8 ls
90/60mmPg. Pls hearL raLe ls 30 beaLs/mln. WhaL ls Lhe malnsLay of Lherapy?
A. lv flulds
8. uobuLamlne
C. Splne moblllzaLlon
u. AnLlbloLlcs
1hls paLlenL ls baslcally sufferlng from neurogenlc shock, so here lv flulds are Lhe malnsLay of
Lherapy.
uobuLamlne ls no doubL very lmporLanL buL lL only works Lo enhance Lhe cardlac ouLpuL
whereas lv flulds lncrease blood volume and also correcL dehydraLlon.
Splne moblllzaLlon ls lmporLanL Loo Lo prevenL furLher Lrauma buL lL alone won'L work.
AnLlbloLlcs are beneflclal and malnsLay of Lherapy when Lhere ls a sepLlc shock. ln Lhls case,
anLlbloLlcs wlll be glven only when Lhere ls a susplclon of lnfecLlon.

A 36-year-old ln[ured male ls presenLed ln emergency wlLh warm exLremlLles, lncreased
resplraLory raLe, ollgurla and rapld pulse. Cn examlnaLlon hls 8.. ls 70/40mmPg, pulse ls
140/mln and Lhere ls blulsh dlscoloraLlon of Llp of nalls and Longue. Whlch klnd of shock ls
developed ln Lhls paLlenL?
Pemorrhaglc Shock
A. SepLlc shock
8. neurologlc shock
C. AnaphylacLlc shock
u. Pypovolemlc shock
1he cllnlcal flndlngs go wlLh Lhe condlLlon of neurogenlc shock. Slnce paLlenL ls ln[ured, lL ls
posslble he has goL an ln[ury Lo hls splnal cord. 1hls causes loss of sympaLheLlc Lone and
sysLemlc vasodllaLlon due Lo unopposed vagal acLlvlLy.
SepLlc shock occurs when Lhere ls a hlsLory of lnfecLlon. ln Lhls condlLlon perlpherles are usually
cold.
AnaphylacLlc shock ls due Lo severe allerglc reacLlon and ls manlfesLed wlLh a rash, lLchlng,
swelllng, low 8 and shorLness of breaLh.
Pypovolemlc shock ls Lhe resulL of bleedlng or hemorrhage anywhere from Lhe body. AlLhough,
Lhls paLlenL ls ln[ured, ln[ury can cause lnLernal bleedlng buL hls perlpherles are warm lnsLead of
belng cold.

A paLlenL has devolved neurogenlc Shock shorLly afLer geLLlng an ln[ury Lo Lhe splnal cord. Pow
wlll he be presenLed cllnlcally?
A. Cold & clammy perlpherles
8. lncreased hearL 8aLe
C. lncreased LoLal perlpheral reslsLance (18)
u. none of Lhese
1he correcL opLlon ls u. 1he perlphery ls usually warm because of sysLemlc vasodllaLaLlon.
PearL raLe ls decreased due Lo loss of sympaLheLlc acLlvlLy and also LoLal perlpheral reslsLance
(18) ls decreased.
Title: Patent Ductus Arteriosus

Objectives for learning: Definition, Pathophysiology, Murmur of PDA, Clinical Symptoms and
Signs, Treatment.

Definition:
Patents means opened
Duct means artery

During fetal development, there is an open space between the pulmonary artery (PA) and the
aorta. It is known as PDA. Blood actually gets shunted from PA into the aorta because lungs are
not developed.


Pathophysiology
Normally blood goes to the right atrium to right ventricle and that blood shunts through
pulmonary artery. The pulmonary artery shunts blood to the lungs which comes back to left
atrium to aorta to rest of the body.

When the baby borns, and takes deep breathe, the resistance inside the lungs decreases and they
expand and opened up. Afterward, there is no need of ductus to shunt blood. It becomes
ligamentum arteriosum.
The problem arises when aorta starts to work and pumps blood into the circulations and the lungs
expand as the baby borns, the resistance inside the lungs decreases, the blood starts to shunt from
left aorta into the pulmonary circulation because pressure in aorta is very high i.e. blood now
shunts from left to right (aorta to pulmonary artery). Now the right ventricle has to pump blood
against higher pressure. Thus, a patient with patent ductus arteriosus develops right ventricular
hypertrophy because the pressure gradients of the right ventricle are higher so to pump blood
against the higher pressure of PA.
As the blood enters into the lungs, they develop vasoconstrictions inside the lungs and therefore
increasing the pulmonary pressures.

Overtime the pulmonary vascular hypertension causes pulmonary vascular sclerosis inside the
pulmonary vasculature. When the pressure inside the RV is high enough, the patients will now
be able to reverse this flow and starts to shunt this deoxygenated blood from right side to left
side. The deoxygenated blood mixes with oxygenated, causing the patient to become cyanosed
and exhausted.

Murmur of PDA

The murmur of PDA is machinery murmur.

! Prostaglandins (PGE) keep PDA open.

Clinical Symptoms And Signs
Symptoms of cyanosis in the lower extremities

Diagnosis

Treatment
It is important to close this PDA. Indomathacin helps to close this PDA.

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234%-#"5%1 67/ $%,/8"89& ueflnlLlon, Causes, aLhophyslology, Cllnlcal sympLoms and slgns,and
ulagnosls

0%6"8"#"78&

8heumaLlc PearL ulsease ls Lhe consequence of Lhe pharyngeal lnfecLlon.

:,*1%1; ("1< 6,-#7/1&
Croup A beLa hemolyLlc SLrepLococcus

=,#)7>)?1"7$79?

1hls ls a Lype ll lmmune medlaLed hypersenslLlvlLy. aLlenLs wlLh Lhls dlsease develop a
murmur. 1hey have vegeLaLlon and flbrosls. 1he mosL affecLed valve ls Lhe mlLral valve. ln case
of acuLe dlsease Lhe anLlbodles of Lhe M proLeln of Lhe organlsm desLroy Lhe valve. 1he
anLlbodles come and blnd Lo M proLeln of Lhe organlsm. 1hey Lhen boLh aLLack and desLroy Lhe
valve causlng an lnflammaLlon.

ln case of acuLe lnflammaLory response on mlLral valve, Lhe paLlenL suffers from mlLral
regurglLaLlon. 1hese proLeln aLLack Lhe glycoproLelns of Lhe anLlgen presenL on Lhe valve.

ln case of chronlc dlsease, flbrosls of Lhe mlLral valve occurs causlng sLenosls of Lhe mlLral valve.
noL only mlLral valve geLs affecLed buL also aorLlc valve can be affecLed. Llkewlse, Lrlcuspld
valve can also geL affecLed. Powever, mlLral and Lhe aorLlc valve geL affecLed more as compared
Lo oLhers.

aLlenLs wlLh rheumaLlc hearL dlsease also develop myocardlLls.

:$"8"-,$ 1?+>#7+1 ,8@ 1"981
lever (101.2 l)
LryLhema marglnaLum (a red margln rash)
valvular damage (paLlenLs develop murmur due Lo vegeLaLlon of Lhe valves. 1he mosL
affecLed valve whlch ls affecLed ls Lhe mlLral valve)
LryLhrocyLe sedlmenLaLlon raLe ls very hlgh
8ed hoL [olnLs ([olnLs paln-mlgraLory polyarLhrlLls)
Sub-cuLaneous nodules (Ashoff bodles: 1hese are Lhe granuloma wlLh hlsLocyLes wlLh glanL
cells)
SalnL vlLus dance or Sydenham's chorea

Sydenham's chorea ls due Lo Lhe CnS paLhology. 1he paLlenL has an lmmune reacLlon. 1he
anLlbodles blnd Lhe neurons ln Lhe braln and Lhus affecL Lhe caudaLe nucleus and subLhalamlc
nuclel. CaudaLe nucleus ls lmporLanL ln Lhe body movemenL.

0",9871"1

ASC: anLlsLrepLolysln C LlLers

!/%,#+%8#

!"#$%& ()*!+, (-.,/

Cb[ecLlves for learnlng: ueflnlLlon, Causes/ 8lsk facLors, aLhophyslology, CompllcaLlons,
SympLoms, ulagnosls and 1reaLmenL of sepLlc shock.

0%1"2"#"32&
1he sepsls paLhway
SysLemlc lnflammaLory response syndrome (SS8l) (l.e. lnflammaLlon and source) ! sepsls (one
organ fallure)! severe sepsls (sepsls plus end organ damage)! sepLlc shock >2 !MCuS

SysLemlc lnflammaLory response syndrome ls deflned as fever of more Lhan 38C and hlgher
hearL raLe.
Sepsls ls Lhe sysLemlc lnflammaLory response syndrome and Lhe presence of a known
lnfecLlon.
SepLlc shock ls perslsLenL hypoLenslon desplLe glvlng lv flulds or vasopressors. lL ls Lhe mosL
common cause of deaLh ln lCu.

,456%67 8"69 14:#3;6&
8acLerlal lnfecLlon by bacLerla such as
! L.Coll
! klebslalla
! SLaph aureus
! seudomonas

*4#<3=<>6"3$3?>
As Lhe bacLerla enLer Lhe blood, lL leads Lo acLlvaLlon of neuLrophlls, monocyLes, lnLerleukln and
cyLoklnes. 1hey rush Lhe blood sLream Lo aLLach Lhe bacLerla. 8acLerla possess dlfferenL
endoLoxlns. 1hese Loxlns damage Lhe endoLhellal cells walls and also acLlvaLe Lhe macrophages,
lnLerleuklns, cyLoklnes, and neuLrophlls leadlng Lo sysLemlc vasodllaLlon. 1hls sysLemlc
vasodllaLlon furLher causes hypoLenslon and underperfuslon of Lhe Llssues causlng lacLlc
acldosls. CoagulopaLhy occurs as Lhe endoLhellum of Lhe blood vessels geLs damaged by Lhe
Loxlns. LvenLually body organs begln Lo damage or organ fallure ensues. 8acLerlal lnfecLlon and
sepsls lead Lo decrease sysLemlc vascular reslsLance and cardlac ouLpuL lncreases Lo
compensaLe Lhls.

Sepsls parameLers lnclude: decreased sysLemlc vascular reslsLance, lncreased cardlac ouLpuL
and decreased caplllary pulmonary wedge pressure.

1. Sl8S
ln Lhls condlLlon followlng lmporLanL flndlngs are presenL:
lever > 38C or <36C
P8 and pulse > 90 beaLs/mln
1achypnea (develops due Lo lacLlc acldosls and so Lo blow ouL excess CC
2
lL leads Lo
hypervenLlllaLlon) 8esplraLory 8aLe ls greaLer Lhan 20 whole CC
2
ls less Lhan 32 mmPg.
W8C > 12,000 cells/ml or <4000 cells/ml or 10 band (lf person ls lmmunocompromlse).
1here may Lherefore be leukocyLosls or leukopenla.

2. Sepsls
lL ls deflned as Sl8S (fever and lncreased hearL raLe) plus lnfecLlon source. lL can be undersLood
by followlng:
lever and neck rlgldlLy- lL means person ls sufferlng from menlnglLls
lever and producLlve cough- slgnlfy pneumonla
lever and flank paln--- deflne Lo be pyelonephrlLls
lever and redness - glve hlnL for cellullLls
lever and rlghL upper quadranL paln - lL means person ls sufferlng from ascendlng cholanglLls.

3. Severe Sepsls
Severe sepsls ls explalned as:
LacLaLe levels > 4mm/dl
Cllgurla <0.3 ml/kg/hour
Change ln menLal sLaLus such as confuslon or leLharglc
MolLed skln
1hrombocyLopenlc < 100,000 leadlng Lo coagulopaLhy
A8uS ln[ury

,3@=$":4#"326
AcuLe resplraLory dlsLress syndrome (A8uS)
ulssemlnaLed lnLravascular coagulaLlon (ulC)
AcuLe Lubular necrosls (A1n)
MulLl organ dysfuncLlon syndrome (MCuS)
ueaLh

,$"2":4$ 6>@=#3@6 42A 6"?26
PypoLenslon
Cllgurla
Warm skln
fever

0"4?236"6
Sepsls ls dlagnosed on Lhe basls of Cllnlcal plcLure l.e. based on sympLoms &
8lood culLures

!;%4#@%2#
lnLravenously broad specLrum anLlbloLlcs are glven aL maxlmum dose.
lf Lhere ls abscess Lhen surglcal dralnage ls used.
lv flulds admlnlsLraLlon ls musL and lmporLanL. normal sallne ls usually glven lnLravenously.
vasopressors are also admlnlsLered Lo supporL perfuslon and hearL. 1hese lnclude
dopamlne, uubuLamlne or noreplnephrlne. uopamlne ls glven Lo lncrease renal perfuslon

B5"C
1. A prevlously healLhy 33 year old man presenLs Lo emergency wlLh sepLlc shock secondary Lo
cellullLls of Lhe arm. Pe ls sllghLly confused and hls perlpherles are cold. Pls hearL raLe ls
123/mln, 8 70/30 mmPg, and resplraLory raLe 23/mln. WhaL should be Lhe mosL sulLable
flrsL llne managemenL ln Lhls case?
A. SLerolds
8. Analgeslcs
C. 8road specLrum anLlbloLlcs
u. AnLlpyreLlcs
ln Lhls case Lhe mosL sulLable flrsL llne managemenL ls Lhe broad specLrum anLlbloLlcs. 1he
raLlonale behlnd ls LhaL Lhls paLlenL has a prevlous hlsLory of cellullLls and due Lo whlch he has
now developed a shock. So Lo combaL Lhe lnfecLlon, anLlbloLlcs are essenLlal.
SLerolds are usually noL glven or glven only when Lhere ls a presence of lnflammaLlon.
Analgeslcs are noL used here as paLlenL has noL complalned of any klnd of paln.
AnLlpyreLlcs are glven Lo LreaL fever buL Lhese are noL Lhe flrsL llne of managemenL of sepLlc
shock.

2. A febrlle paLlenL was dlagnosed wlLh L. coll sepsls. ShorLy, he develops sepLlc shock. Whlch
of Lhe glven opLlon ls responslble for Lhls reacLlon?
A. 8acLerlal surface anLlgens causlng sLlmulaLlon of a humoral lmmune response
8. A cell-medlaLed lmmune response Lo L.coll
C. CyLoklnes secreLlon by monocyLes as a resulL of sLlmulaLlon by endoLoxln
u. Cranule conLenLs released by basophlls and masL cells
L. 8acLerlal superanLlgen Loxln causlng acLlvaLlon of 1P cells
1he correcL answer ls: C.
1he correcL opLlon ls C. cyLoklnes are responslble for Lhe occurrence of sepLlc shock. CyLoklnes
are secreLed by Lhe monocyLes owlng Lo Lhe sLlmulaLlon by Lhe bacLerlal endoLoxlns. CyLoklnes
are baslcally lmmunomodulaLlng agenLs.
8acLerlal surface anLlgens causlng sLlmulaLlon of a humoral lmmune response does noL lead Lo
Lhls plcLure buL Lhe Loxln produced by L.coll ls responslble for sepLlc shock.
A cell-medlaLed lmmune response also Lakes place Lo L.coll buL agaln lL does noL glve rlse Lo
sepLlc shock. Cell medlaLed lmmunlLy ln facL offers proLecLlon agalnsL ma[orlLy of lnLracellular
bacLerlal paLhogens.
Cranule conLenLs released by basophlls and masL cells do noL lead Lo sepLlc shock. lnsLead
anaphylacLlc shock may occur lf Lhere ls severe allerglc reacLlon Laken place.
8acLerlal superanLlgen Loxln causlng acLlvaLlon of 1P cells leads Lo release of cyLoklne buL can
produce Lhe plcLure of 1oxlc Shock Syndrome noL Lhe sepLlc shock.

3. A paLlenL wlLh sepLlc shock develops hypoLenslon. WhaL ls Lhe cause behlnd hypoLenslon?
A. lncreased caplllary permeablllLy and masslve vasodllaLlon
8. uecreased sysLemlc vascular reslsLance and vasoconsLrlcLlon
C. uecreased caplllary permeablllLy
u. Masslve vasoconsLrlcLlon
lncreased caplllary permeablllLy and masslve vasodllaLlon are boLh held responslble for
produclng hypoLenslon ln sepLlc shock. 1he lncrease ln caplllary permeablllLy as well as
vasdllaLlon occurs as a resulL of lnflammaLory medlaLors affecLlng Lhe caplllarles. 1he sysLemlc
lmmune response Lo mlcroblal lnfecLlon brlngs abouL venous blood poollng and arLerlal
vasodllaLlon.
vasoconsLrlcLlon does noL occur here lnsLead vasodllaLlon Lakes place. 1he perlpheral vascular
reslsLance ls however decreased here.
Caplllary permeablllLy ls noL decreased buL lL ls lncreased due Lo sysLemlc lmmune response Lo
endoLoxlns.
Masslve vasoconsLrlcLlon ls noL posslble so Lhls opLlon ls noL correcL.
4. A paLlenL presenLs wlLh confuslon. Pe has a hlsLory of fever and vomlLlng for 3 days. Cn
examlnaLlon hls skln ls warm, neck ls rlgld, pulse ls 120/mlnuLe and 8 ls 90/70mmPg. WhaL
ls Lhe mosL probable dlagnosls?
A. MenlnglLls
8. Sepsls and menlnglLls
C. Sepsls
u. neurogenlc shock
1he cllnlcal plcLure goes wlLh Lhe dlagnosls of sepsls and menlnglLls. lever, vomlLlng and neck
rlgldlLy show lncreased lnLracranlal pressure. 1hls ls mosL llkely due Lo menlnglLls whlle
confuslon, decreased 8, hoL flushed skln and lncreased hearL raLe show Lhe occurrence of
sepsls (l.e. fever and source of lnfecLlon).
AlLhough menlnglLls ls presenL buL Lhere ls an elemenL of sepsls as well so alone menlnglLls ls
noL a correcL opLlon.
Llkewlse, sepsls alone ls noL correcL slnce Lhere ls a clear plcLure of menlnglLls.
neurogenlc shock may presenL wlLh decreased 8, buL hlsLory of fever ls unllkely. Powever,
Lhere ls a hlsLory of Lrauma Lo back or splnal cord. AddlLlonally, skln of Lhe paLlenL ls usually
cold here due Lo hypoLenslon.

3. A paLlenL presenLs wlLh molLed skln, ollgurla, hypoLenslon, confuslon, elevaLed lacLaLe and
purpura all over Lhe skln. WhaL would be compllcaLlon of sepsls causlng Lhese problems?
A. AcuLe resplraLory dlsLress syndrome (A8uS)
8. MeLabollc acldosls
C. SysLemlc lnflammaLory response syndrome (Sl8S)
u. MulLl organ dysfuncLlon syndrome (MCuS)
1he correcL answer ls: u
MolLed skln, ollgurla, hypoLenslon, confuslon, elevaLed lacLaLe and purpura all over Lhe skln
demonsLraLe Lhe occurrence of mulLl organ dysfuncLlon syndrome (MCuS). lL ls one of Lhe mosL
common compllcaLlon LhaL affecL dlfferenL organs of Lhe body.
lf an acuLe resplraLory dlsLress syndrome (A8uS) occurs, Lhen paLlenL complalns of shorLness of
breaLh or dlfflculL breaLh.
MeLabollc acldosls does noL produce Lhese sympLoms. lL may presenL wlLh headache, paln ln
chesL, palplLaLlons, weakness, eLc.
SysLemlc lnflammaLory response syndrome (Sl8S) ls an lnflammaLory condlLlon affecLlng Lhe
whole body, and ls malnly a response of Lhe body's lmmune sysLem Lo lnfecLlon. 1emperaLure ls
elLher hlgh or low, Lhere ls Lachypnea and lncreased hearL raLe. Cllgurla, hypoLenslon,
confuslon, elevaLed lacLaLe and purpura are noL presenL here.

!"#$%$&" ()#" *$(+,"

"#$%&' ($)*%& +,-#,)

.*/&0$#1&2 345 %&)5,#,-' Leaining pathophysiological anu clinical featuies of stable
angina; unueistanuing the impoitance of coiiect uiagnosis anu tieatment.

6&3#,#$#4,2' Stable angina is an imbalance between bloou flow thiough the
coionaiy aiteiies anu oxygen uemanu.

7)82&29 :#2; 3)0$452'
Acionym: FLASB - NB
Family histoiy of coionaiy uisease
Low BBL (<4u)
Age (men>4S, women>SS)
Smoking
Bypeitension
Nale genuei
Biabetes

<)$=4>=?2#4%4-?'
Bue to atheioscleiotic plaques that occluue the lumen of coionaiy aiteiies, theie is
a highei uemanu foi oxygen than it coulu be ueliveieu thiough the occluueu
aiteiies. Becieaseu peifusion to the heait muscle causes ischemia of the
myocaiuium piesenteu with chest pain, especially uuiing the exeicise.

7%#,#0)% 2?@>$4@2 ),A 2#-,2
Chest pain
Exeition
Symptoms can last foi 1u - 1S min, but usually 1-S min.
Symptoms aie ielieveu by iest anu sublingual nitioglyceiin
6#)-,42#2
EKu (noimal finuings)
Caiuiac enzyme (no elevation)
Stiess test
o Exeicise (tieaumill) - until the maximum heait iate is ieacheu (22u -
age)
! Chest pain
! Bypotension
! ST-uepiession
! Aiihythmia
o Stiess echo
Caiuiac catheteiization - if stiess test is positive.
Phaimacologic stiess test (foi patients that aie not able to peifoim exeicise)
o Iv auenosine (causes coionaiy vasouilatation)
o Bipyiiuamol (causes coionaiy vasouilatation)
o Bobutamine (incieases myocaiuial oxygen uemanu; incieases heait
iate, contiactility, anu bloou piessuie)

74@>%#0)$#4,2
Piogiession of stable angina leaus to acute coionaiy synuiome (unstable angina,
non-STENI, anu STENI)

"5&)$@&,$
Risk factoi mouification
o Biet (<7% satuiateu fat; <2uu mguay cholesteiol)
o Exeicise
o Lose weight
o Stiict bloou glucose contiol
o Statins
o Bloou piessuie contiol
o Stop smoking
Neuication
o Aspiiin
o Beta-blockeis
o Nitiates
Revasculaiization
o PTCA (peicutaneous tiansluminal coionaiy angioplasty) - stent
implantation
o Coionaiy bypass
Title: Tricuspid Regurgitation
Objectives for learning: Definition, Causes/ Risk factors, Clinical symptoms and signs and v

Definition:
It is the inability of three valves (tricuspid valves) to close completely during systole.

The most common cause is right ventricular dilation. Other causes include:
Left ventricular failure
Right ventricular infraction
Cor pulomonale (pulmonary hypertension)
Staph aureus infection
Ebstein anomaly (congenital heart disease)
Carcinoid syndrome

Pathophysiology:

Clinical symptoms and signs:

Ascites: Jugular Venous Distention, heptomegaly
Pulsatile liver
Blowing holo-systolic murmur: When patient is asked to deep breath, the murmur is heard
louder.
Atrial fibrillation

Diagnosis:

Treatment:
Treat the underlying cause
Surgery involve valve repairmen or valvuloplasty
Quiz
1. A patient came with leg edema and swollen abdomen. On examination jugular vein was
found to be distended, ascites were present and liver was enlarged and pulsatile. What is the
most likely diagnosis?
A. Aortic stenosis
B. Pulmonary stenosis
C. Tricuspid regurgitation
D. Mitral regurgitation
The most likely diagnosis based on the clinical symptoms and signs is the tricuspid regurgitation.
In this condition tricuspid valve fails to close during systole, causing the blood to passes with
each heart beat from the right ventricle to the right atrium, i.e. in the direction opposite to that of
the normal one. Symptoms of right-sided heart failure often develop. Jugular vein is usually
distended. The important finding of tricuspid regurgitation is the pulsatile liver. It is not present
in the other conditions mentioned in the options.
Aortic stenosis is the condition of narrowing of the aortic valve. It may present with pedal,
exertional dyspnea, paroxysmal nocturnal dyspnea, but liver is not pulsatile here.
Pulmonary stenosis is the condition of obstruction of blood flow from the right ventricle to
the pulmonary artery. Due to this right ventricular hypertrophy develops. There may be
complaint of chest pain, palpitations, dysnpea but liver is not pulsatile.
Mitral regurgitation is characterized by the symptoms of decompensated congestive heart failure.
Liver here is not pulsatile but normal.

2. Which of the given option is associated with pansystolic murmur?

A. Aortic stenosis ejection systolic
B. Pulmonary stenosis
C. Tricuspid regurgitation
D. Pulmonary regurgitation decrescendo diastolic murmur

Tricuspid regurgitation is associated with pansystolic murmur. This type of murmur is of low
frequency and shows tendency to increase with inspiration.

Aortic stenosis is associated with ejection systolic murmur.

The murmur of pulmonary stenosis is systolic murmur.
Pulmonary regurgitation is associated with decrescendo diastolic murmur.
3. Identify the condition in which pulsatile liver is found?
A. Tricuspid regurgitation
B. Mitral regurgitation
C. Pulmonary hypertension
D. Mitral stenosis

Liver becomes pulsatile in case of tricuspid regurgitation. This condition is responsible for liver
dysfunction.

Mitral regurgitation, pulmonary hypertension and mitral stenosis do not lead to the liver to
become pulsatile. Liver usually remains normal.

4. What is the surgical management of tricuspid regurgitation?

A. Removal of valves
B. There is no surgical treatment of tricuspid regurgitation
C. Only repair of the valve
D. Valve repair (valvuloplasty) or replacement

The surgical management of tricuspid regurgitation is Valve repair (valvuloplasty) or
replacement. The valves are repaired surgically to make them functional.

Valves cannot be removed but can be replaced for the normal functioning of the heart.

The surgical treatment of tricuspid regurgitation is present and is successful.

Valve can be repaired or can be replaced depending upon the condition.

5. A 9-year-old boy is found to have tricuspid regurgitation. What would be most common
cause behind this?
A. Atrial septal defect
B. Ventricular septal defect
C. Ebstein anomaly
D. Carcinoid syndrome

The most common cause in the 9-year-boy is Ebstein anomaly. Ebstein anomaly is a basically a
congenital cardiac defect characterized by the displacement of septal leaflet of the tricuspid
valve towards the right ventricular apex.

Atrial septal defect is not presented with the tricuspid regurgitation. It is basically a defect
between the two atria, right and left, causing the oxygenated blood to mix with the deoxygenated
blood.

Ventricular septal defect as the name implies is the congenital anomaly characterized by the
presence of defect ventricular septum. This condition is not presented with tricuspid
regurgitation. If defect is small, it remains asymptomatic or disease usually becomes apparent a
few weeks after birth.

Carcinoid syndrome is the complex of different symptoms such as diarrhea, dysnpea, flushing,
palpitations etc. this syndrome is due to carcinoid tumor. Although tricuspid regurgitation occurs
in carcinoid syndrome but in this patient, no such history is there regarding the symptoms of
carcinoid syndrome. Also, this syndrome is more common in adults. Thus, it is not considered a
correct option here.

!"#$%& ()*%+,#-)*"). !/% 0-,"1, 23 4/516
Cb[ecLlves for learnlng: ueflnlLlon, 1ypes, CompllcaLlons, SympLoms, ulagnosls and 1reaLmenL
of shock.
7%3")"#"5)&
Shock ls Lhe under perfuslon of Lhe Llssues. 8lood flow ls lmporLanL for Lhe normal funcLlonlng
of Lhe braln, hearL, kldney, llver, muscles and dlfferenL oLher body Llssues. 8lood dellvers
oxygen, nuLrlenLs and glucose needed for meLabollsm. lL ls a serlous medlcal emergency and
Lherefore requlres an lmmedlaLe medlcal lnLervenLlon oLherwlse lL wlll prove faLal lf lrreverslble
organ damage occurs.
arameLers golng Lo be affecLed
Cardlac ouLpuL
SysLemlc reslsLance
ulmonary caplllary wedge pressure
8-9,%,: ;",6 3-1#5+,&
<-#/5=/>,"5$5.>
8$")"1-$ ,>?=#5?, -)* ,".),
PypoLenslon (low 8)
Cllgurla
1achycardla
85?=$"1-#"5), 53 4/516,
LacLlc acldosls (anaeroblc resplraLlon)
Cllgurla (decreased urlne ouLpuL)
CnS dysfuncLlon (alLered menLal sLaLus)
!>=%, 53 4/516
neurogenlc shock
Cardlogenlc shock
AnaphylacLlc shock
SepLlc shock
Pypvolemlc shock
7"-.)5,",: @==+5-1/ #5 ,/516
PlsLory: lf Lhere ls hlsLory of fever and low 8, lL shows lnfecLlon (lL may be a sepLlc shock).
lf Lhere ls hlsLory of Lrauma, Cl bleed, vomlLlng, or dlarrhea, lL means volume depleLlon has
occurs so hypovolemlc shock ls posslble.
lf Lhere ls complalnL of chesL paln and low 8 and cardlac ouLpuL ls decreased, a person may be
havlng acuLe myocardlal lnfarcLlon (Ml), Lhen lL wlll be a cardlogenlc shock.
ln case of neurologlc shock Lhere wlll be neurologlc deflclL.

lv lnfuslons ls lmporLanL and glven wlLh 2 large bored lv llnes. A fluld of abouL 300 Lo 1000 ml
should be glven for organ perfuslon.

A-B, ")1$9*%& blood sampllng for C8C, 1/A11, 8l1s (8un/CreaLlnlne) and 8M
CDE& 1o check Lhe presence of S1 elevaLlon, depresslon or oLher posslble flndlngs
8/%,# FG+->& lL wlll help ln ldenLlfylng Lhe chronlc hearL fallure (CPl), cardlomegaly, Lenslon
pneumoLhorax
<9$,% 5H"?%#+>& lL should be 100

vasopressors are glven such as dopamlne, dubuLamlne and noreplnephrlne.
!+%-#?%)#
1he baslc and mosL lmporLanL early LreaLmenL of shock lnvolves:
A8C
l.e.
MalnLaln alrways
8reaLhlng
ClrculaLlon

CLher LreaLmenL varles dependlng on Lhe Lype of shock and lLs causes.

I9"J
1. A 14-year-paLlenL presenLs wlLh fever, confuslon and weakness. Cn examlnaLlon he ls pale
wlLh weak Lhread pulse. Pls LemperaLure ls 102l. Pls aLLendanL Lells LhaL paLlenL has been
sufferlng from flank paln for 4 days before. Pls 8 ls 80/60mmPg. WhaL ls Lhe mosL llkely
dlagnosls?
A. AcuLe kldney ln[ury
8. Shock
C. Adrenal Crlsls
u. 1oxlc Shock Syndrome
1hls paLlenL ls a Lyplcal case of shock, mosL probably Lhe sepLlc shock. 1hls ls because Lhere ls a
hlsLory of flank paln and fever. Pls LemperaLure ls also ralsed. Low 8 and alLered menLal sLaLus
lndlcaLe LhaL he has developed a shock.
AcuLe kldney ln[ury ls noL presenLed wlLh low 8. lL ls presenLed mosLly wlLh hlgh 8 and Lhere
ls generallzed edema. aLlenL complalns of headache and vomlLlng.
Adrenal Crlsls ls characLerlzed by severe adrenal lnsufflclency due Lo lnadequaLe levels of
corLlsol ln Lhe body. 1here ls alLhough sympLoms of confuslon, fever, and low 8 buL Lhere ls a
wlde range of meLabollc abnormallLles such as hyperkalemla, hypercalcemla, hypoglycemla and
hyponaLremla.
1oxlc shock syndrome (1SS) ls a acuLe llfe-LhreaLenlng condlLlon medlaLed by bacLerlal Loxln
usually by elLher !"#$%&'()())*+ #*-.*+ or !"-.$"()())*+. lL ls characLerlzed by rash, hlgh fever,
desquamaLlon hypoLenslon, and mulLl-organ fallure. lL ls presenLed wlLh severe myalgla,
headache, dlarrhea, vomlLlng, and non-focal neurologlc deflclL.

2. ln a paLlenL wlLh reduced cardlac ouLpuL and low 8 wlLh Lhe dlagnosls of shock, whaL
would be Lhe besL LreaLmenL opLlon Lo boosL cardlac ouLpuL?
A. lv llulds
8. 8eLa 8lockers
C. AnLlbloLlcs
u. vasopressors
1he besL LreaLmenL opLlon Lo enhance Lhe cardlac ouLpuL and low 8 ln paLlenL wlLh shock ls
Lhe vasopressors. 1hese drugs work by lncreaslng Lhe 8, conLracLlllLy of Lhe hearL as well as Lhe
renal perfuslon.
lv flulds are alLhough musL here buL someLlmes Lhey fall Lo lncrease Lhe 8 and cardlac ouLpuL.
8eLa 8lockers have no role ln lncreaslng Lhe hearL raLe or blood pressure, ln facL Lhey reduce
blood pressure and Lachycardla.
AnLlbloLlcs are usually prescrlbed when Lhere ls any evldence of lnfecLlon. 1hey have no role ln
lncreaslng Lhe cardlac ouLpuL and 8.
3. Whlch of Lhe glven feaLure helps Lo dlfferenLlaLe Lhe hypovolemlc shock from sepLlc shock?
A. 8lood pressure
8. Cardlac CuLpuL
C. 1emperaLure
u. PearL raLe
8ody LemperaLure ls Lhe dlfferenLlaLlng feaLure ln case of Lhe hypovolemlc shock and sepLlc
shock. ln hypvolemlc shock LemperaLure ls reduced so paLlenL's skln ls cold whlle ln sepLlc shock
due Lo lnfecLlon LemperaLure ls ralsed so skln ls warm.
8lood pressure and cardlac ouLpuL boLh are reduced ln boLh hypvolemlc and sepLlc shock. So
Lhese parameLers cannoL help ln dlfferenLlaLlng.
Llkewlse, hearL raLe ls also lncreased ln boLh shock Lherefore, lL won'L help ln conflrmlng
wheLher a paLlenL ls sufferlng from hypovolemlc and sepLlc shock.
4. A paLlenL presenLs wlLh Lhe progresslve sLage of shock. WhaL wlll happen wlLh Lhe
meLabollsm of paLlenLs lf Lhe shock ls noL LreaLed and hypoxla of Lhe Llssue occurs?
A. CompensaLory mechanlsms
8. LacLlc acldosls
C. ArLerlolar consLrlcLlon due Lo vasomoLor reflex
u. MeLabollsm wlll be unaffecLed
A paLlenL wlLh Lhe progresslve sLage of shock, lf noL LreaLed and developed hypoxla of Lhe
Llssue, mosL llkely enLers lnLo anaeroblc meLabollsm and Lherefore develops lacLlc acldosls.
CompensaLory mechanlsms are already worklng well before Lhe person enLers lnLo progresslve
shock, so Lhls opLlon ls noL correcL.
ArLerlolar consLrlcLlon due Lo vasomoLor reflex ls agaln already worklng here Lo compensaLe.
MeLabollsm wlll be affecLed here when oxygen dellvery and nuLrlenLs are noL sufflclenL so Lo
compensaLe aeroblc meLabollsm shlfLs Lo anaeroblc.
3. A paLlenL presenLs wlLh confuslon afLer severe bleedlng ln Lhe vomlLlng. Pe has developed
Lachycardla whlle hls pulse ls weak. Whlch klnd of shock ls assoclaLed wlLh low levels of
blood?
8. AnaphylacLlc shock
C. Cardlogenlc shock
u. SepLlc shock

1he correcL answer ls A
Pypovolemlc shock ls assoclaLed wlLh low levels of blood and ls characLerlzed by bleedlng or
hemorrhage.
AnaphylacLlc shock ls assoclaLed wlLh allerglc reacLlon Lo drug, chemlcal, eLc and ls Lhe serlous
sorL of allerglc reacLlon.
Cardlogenlc shock ls characLerlzed by dlfferenL condlLlons affecLlng Lhe hearL causlng Lhe hearL
dlfflculL Lo pump Lhe blood as Lhe body requlres.
SepLlc shock occurs afLer Lhe lnfecLlon/bacLerla enLer lnLo Lhe blood sLream and ls an exLreme
response by Lhe lmmune sysLem.

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Ftplectures Cardiovascular system Lecture Notes

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